Alergie
Patofizjologia i mechanizm

Alergie są schorzeniami systemowymi wynikającymi z nieprawidłowej, nadmiernej odpowiedzi układu immunologicznego na nieszkodliwe dla większości alergenów. Patogeneza obejmuje fazę sensytyzacji, w której komórki dendrytyczne prezentują antygen limfocytom TH2, prowadząc do produkcji specyficznych przeciwciał IgE, które wiążą się z receptorami FcεRI na komórkach tucznych. Ponowna ekspozycja na alergen powoduje degranulację mastocytów i uwolnienie mediatorów zapalnych, głównie histaminy, leukotrienów i cytokin (IL-4, IL-5, IL-13), co wywołuje natychmiastową reakcję alergiczną oraz późną fazę z udziałem eozynofilów i innych komórek zapalnych. W patogenezie kluczową rolę odgrywają także predyspozycje genetyczne, środowisko, mikrobiota jelitowa oraz zaburzenia równowagi immunologicznej między komórkami TH1 i TH2. Fenotypy kliniczne obejmują alergiczny nieżyt nosa, astmę alergiczną, atopowe zapalenie skóry i alergię pokarmową, z różnorodnością mechanizmów molekularnych i immunopatologicznych.

Patogeneza alergii

Alergie to schorzenia systemowe spowodowane zaburzeniem funkcjonowania układu immunologicznego. Są one wynikiem nieprawidłowej, nadmiernej reakcji układu odpornościowego na substancje, które dla większości osób są nieszkodliwe, nazywane alergenami12. Mechanizm patogenetyczny chorób alergicznych jest złożony i obejmuje wiele czynników, w tym środowisko matczyno-płodowe, środowisko życia, predyspozycje genetyczne, czynniki epigenetyczne oraz stan układu odpornościowego organizmu34.

Historia rodzinna alergii jest najważniejszym pojedynczym czynnikiem, który zwiększa ryzyko rozwoju chorób alergicznych5. Osoby z predyspozycjami genetycznymi do atopii (genetyczna skłonność do wytwarzania przeciwciał IgE w odpowiedzi na alergeny) mają podwyższone poziomy IgE i eozynofilów we krwi6.

Mechanizm reakcji alergicznej

Reakcje alergiczne są inicjowane, gdy alergeny krzyżowo łączą się z preformowanymi przeciwciałami IgE związanymi z receptorami o wysokim powinowactwie FcεRI na powierzchni komórek tucznych (mastocytów)7. W początkowych stadiach alergii, reakcja nadwrażliwości typu I przeciwko alergenowi napotkanemu po raz pierwszy i prezentowanemu przez profesjonalną komórkę prezentującą antygen powoduje odpowiedź limfocytów TH2, które produkują cytokinę zwaną interleukiną-4 (IL-4)8.

Mechanizm rozwoju alergii można podzielić na dwa główne etapy: fazę sensytyzacji i fazę efektorową.

Faza sensytyzacji

Gdy osoby predysponowane genetycznie do atopii napotykają alergeny, dochodzi do procesu sensytyzacji (uczulenia). Komórki dendrytyczne wychwytują i przetwarzają alergeny, przekazując informacje o antygenie limfocytom T pomocniczym, co prowadzi do zaburzenia równowagi immunologicznej i polaryzacji w kierunku odpowiedzi TH29. Te specyficzne dla antygenu komórki TH2 prezentują informacje o alergenie limfocytom B i kierują ich różnicowanie w kierunku komórek plazmatycznych wytwarzających specyficzne dla alergenu przeciwciała IgE10.

Wytwarzane przeciwciała IgE wiążą się z receptorami o wysokim powinowactwie (FcεRI) na powierzchni komórek tucznych, co prowadzi do ich uczulenia11. Ta pierwsza faza, znana jako „sensytyzacja”, nie powoduje jeszcze żadnych objawów12.

Faza efektorowa – wczesna i późna odpowiedź alergiczna

Gdy uczulone komórki tuczne są ponownie eksponowane na specyficzne alergeny, dochodzi do ich aktywacji i degranulacji, co prowadzi do uwolnienia mediatorów zapalnych13. Odpowiedź alergiczna po aktywacji mastocytów zależnej od IgE występuje jako reakcja natychmiastowa, rozpoczynająca się w ciągu sekund od kontaktu z alergenem, oraz reakcja późna, która rozwija się w ciągu 8-12 godzin14.

Wczesna faza reakcji alergicznej

Aktywowane komórki tuczne i bazofile przechodzą proces degranulacji, podczas którego uwalniają histaminę i inne mediatory zapalne (cytokiny, interleukiny, leukotrieny i prostaglandyny) z ich ziarnistości do otaczających tkanek, powodując kilka efektów ogólnoustrojowych, takich jak rozszerzenie naczyń, wydzielanie śluzu, stymulacja nerwów i skurcz mięśni gładkich15.

Głównym mediatorem tej reakcji jest histamina, która odgrywa kluczową rolę w patofizjologii alergii16. Histamina jest cząsteczką sygnałową, która po uwolnieniu wywołuje objawy alergii poprzez wiązanie się z receptorami H1. Prowadzi to do kaskady obejmującej aktywację białka Gq/11 i sygnalizację fosfolipazy C, wytwarzając DAG i IP3. Ten proces promuje skurcz mięśni gładkich, zwiększa przepuszczalność naczyń i przyczynia się do charakterystycznych objawów reakcji alergicznych, takich jak swędzenie, skurcz oskrzeli i obrzęk tkanek17.

Reakcja natychmiastowa objawia się klinicznie jako pokrzywka, świąd, obrzęk, wyciek z nosa, kichanie, skurcz oskrzeli, a w ciężkich przypadkach – anafilaksja18.

Późna faza reakcji alergicznej

Po ustąpieniu mediatorów ostrej odpowiedzi, mogą wystąpić reakcje późnej fazy. Jest to spowodowane migracją innych leukocytów, takich jak neutrofile, limfocyty, eozynofile i makrofagi, do pierwotnego miejsca reakcji19. Ta późna odpowiedź obejmuje rekrutację innych komórek efektorowych, zwłaszcza limfocytów TH2, eozynofilów i bazofilów, które znacząco przyczyniają się do immunopatologii odpowiedzi alergicznej20.

Charakterystyczną cechą późnej fazy astmatycznej jest naciek dróg oddechowych komórkami zapalnymi i mediatorami, szczególnie eozynofilami, co prowadzi do zwężenia dróg oddechowych i związanej z tym nadreaktywności oskrzeli21. Eozynofile odgrywają ważną rolę w patofizjologii astmy, a ich migracja do płuc wiąże się ze stanem zapalnym i skurczem oskrzeli22.

Podobnie w alergicznym nieżycie nosa, po wczesnej odpowiedzi w nosie następującej po ekspozycji na alergen, komórki zapalne są nadal rekrutowane. Eozynofile odgrywają ważną rolę w późnej fazie odpowiedzi w nosie, a uwalniane przez nie enzymy i białka powodują uszkodzenie tkanek i dalszy stan zapalny23.

Późna faza reakcji alergicznej może ewoluować w przewlekły stan zapalny, charakteryzujący się obecnością efektorowych komórek T i eozynofilów, co jest najwyraźniej widoczne w przewlekłej astmie alergicznej24.

Rola komórek i mediatorów w odpowiedzi alergicznej

Komórki tuczne i bazofile

Komórki tuczne są kluczowymi komórkami efektorowymi w odpowiedzi alergicznej. Są to komórki ziarniste, co oznacza, że zawierają liczne ziarnistości wydzielnicze, które po aktywacji uwalniają swoją zawartość do krwiobiegu25. Komórki tuczne wyścielają powierzchnie ciała i służą do alarmowania układu odpornościowego o lokalnym zakażeniu, ale również odgrywają główną rolę w reakcjach alergicznych26.

W przypadku alergii wiązanie alergenu z przeciwciałami IgE na powierzchni komórek tucznych prowadzi do ich szybkiej degranulacji i uwolnienia związków zapalnych, w tym histaminy, które przyczyniają się do miejscowego stanu zapalnego i objawów związanych z alergią27. Po aktywacji komórki tuczne syntetyzują i uwalniają również chemokiny, mediatory lipidowe, takie jak leukotrieny i czynnik aktywujący płytki (PAF), oraz dodatkowe cytokiny, takie jak IL-4 i IL-13, które podtrzymują odpowiedź TH228.

Eozynofile

Eozynofile są granulocytami, które powstają w szpiku kostnym29. Mają dwa rodzaje funkcji efektorowych. Po pierwsze, po aktywacji uwalniają wysoce toksyczne białka granularne i wolne rodniki, które mogą zabijać mikroorganizmy i pasożyty, ale mogą również powodować znaczne uszkodzenia tkanek w reakcjach alergicznych30.

W lokalnej reakcji alergicznej degranulacja komórek tucznych i aktywacja limfocytów TH2 powodują akumulację eozynofilów w dużej liczbie oraz ich aktywację. Ich ciągła obecność jest charakterystyczna dla przewlekłego zapalenia alergicznego i uważa się, że są one głównymi czynnikami przyczyniającymi się do uszkodzenia tkanek31.

Limfocyty TH2

Odpowiedź immunologiczna zależy od dwóch podgrup limfocytów T, znanych jako komórki T pomocnicze TH1 i TH232. U osób atopowych komórki TH2 i ich mediatory zachęcają układ odpornościowy do rozpoznawania alergenów jako najeźdźców i do montowania przeciwko nim odpowiedzi33.

Komórki TH2 wydzielają cytokiny zapalne, w tym IL-4, IL-5, IL-13, IL-14 i IL-31, które przyczyniają się do rozwoju alergicznego zapalenia34. Cytokiny te regulują aktywację i rekrutację prozapalnych komórek (komórek tucznych i eozynofilów) w narządach docelowych błon śluzowych, a także przełączanie klasy na IgE w komórkach B35.

Równowaga między komórkami TH2 promującymi alergię a komórkami TH1 zwalczającymi infekcje okazała się krytycznym składnikiem naszego układu odpornościowego36. Zaburzenie tej równowagi może prowadzić do rozwoju chorób alergicznych lub autoimmunologicznych, w zależności od natury antygenu37.

Mediatory zapalne

Mediatory zapalne odgrywają kluczową rolę w patogenezie alergii. Najważniejsze z nich to:

  • Histamina – główny mediator wczesnej fazy reakcji alergicznej, powoduje rozszerzenie naczyń, zwiększenie przepuszczalności naczyń, skurcz mięśni gładkich3839
  • Leukotrieny – potężne substancje kurczącej oskrzela, wzmacniające działanie histaminy40
  • Cytokiny (IL-4, IL-5, IL-13) – promują eozynofilię, wydzielanie śluzu i rekrutację komórek zapalnych41
  • Chemokiny – przyciągają neutrofile do miejsca reakcji, co może nasilać stres oksydacyjny w drogach oddechowych42
  • Prostaglandyny i czynnik aktywujący płytki (PAF) – przyczyniają się do reakcji zapalnej43

Czynniki wpływające na patogenezę alergii

Czynniki genetyczne

Predyspozycje genetyczne odgrywają istotną rolę w rozwoju alergii. Historia rodzinna alergii jest najważniejszym pojedynczym czynnikiem, który zwiększa ryzyko rozwoju chorób alergicznych44. Specyficzne warianty genów, które zmieniają kodowanie cytokin pochodzących z komórek nabłonkowych, takich jak interleukina-33 i limfopoetyna zrębu grasicy, mogą być zaangażowane w patogenezę alergii45. Dodatkowo, warianty genów ORMDL3 i GSDML zostały powiązane ze zwiększonym ryzykiem astmy o wczesnym początku46.

Czynniki środowiskowe

Środowisko odgrywa kluczową rolę w rozwoju alergii. Teoria higieny sugeruje, że postęp w higienie, mimo że poprawił długość życia poprzez drastyczne zmniejszenie liczby zgonów z powodu chorób zakaźnych, może przyczyniać się do wzrostu częstości występowania alergii47.

Ekspozycja na alergeny środowiskowe, takie jak pyłki, roztocza kurzu domowego, pleśnie czy alergeny zwierzęce, może prowadzić do sensytyzacji i rozwoju chorób alergicznych u osób predysponowanych genetycznie48. Badania wykazały, że niektóre czynniki środowiskowe, takie jak pewne składniki mikrobiologiczne produkowane przez bakterie, grzyby lub wirusy, mogą stymulować komórki nabłonkowe rogówki do produkcji cytokin, takich jak TSLP (thymic stromal lymphopoietin), które regulują odpowiedź immunologiczną w kierunku odpowiedzi alergicznej typu TH249.

Mikrobiota jelitowa

Mikrobiota jelitowa odgrywa istotną rolę w kształtowaniu narządów układu odpornościowego i pomaga identyfikować wzorce odpowiedzi immunologicznej gospodarza50. Dysbioza, czyli zaburzenie homeostazy jelitowej spowodowane zmianą funkcji i składu mikrobioty, może być czynnikiem w patogenezie różnych zaburzeń, w tym chorób alergicznych51.

Istnieje coraz więcej dowodów na to, że dysbioza poprzedza wystąpienie objawów alergicznych52. Wykazano również, że niektóre bakterie w mikrobiocie specyficznie blokują odpowiedzi immunologiczne zaangażowane w reakcje alergiczne53.

Infekcje wirusowe i bakteryjne

Infekcje wirusowe i bakteryjne mogą mieć wpływ na rozwój chorób alergicznych. Infekcje wirusowe mogą mieć różne, przeciwstawne efekty na rozwój alergii i astmy; w zależności od okoliczności, wirusy mogą albo chronić przed, albo wywoływać zaburzenia alergiczne54.

Bakterie odgrywają podwójną rolę w alergiach – głównie ochronną, chociaż niektóre gatunki bakterii stymulują zapalenie alergiczne55. Ekspozycja na bakterie od dawna była wiązana z zapobieganiem alergiom, co jest podstawą teorii higieny56.

Heterogenność patogenezy chorób alergicznych

Patogeneza chorób alergicznych wykazuje wyraźną heterogenność, przy czym fenotyp i endotyp określają odpowiednio widoczne cechy i powiązane mechanizmy molekularne5758.

Alergiczny nieżyt nosa i astma alergiczna

Profile immunopatologiczne alergicznego nieżytu nosa (AR) i astmy alergicznej (AAS) są bardzo podobne pod względem infiltracji eozynofilów, komórek tucznych i komórek Th259. W przypadku astmy alergicznej zmiany patologiczne błony śluzowej obejmują hiperplazję nabłonka, metaplazję komórek kubkowych i zwiększoną produkcję śluzu60.

Patofizjologia alergicznego nieżytu nosa obejmuje limfocyty pomocnicze Th2 i zapalenie mediowane przez IgE z nadaktywną funkcją adaptacyjnego i wrodzonego układu odpornościowego61. Proces rozpoczyna się, gdy aeroalergen przenika barierę błony śluzowej nosa. Alergen jest następnie fagocytowany przez komórkę prezentującą antygen (APC), która prezentuje antygen naiwnej komórce T CD4+ pomocniczej, stymulując ją do różnicowania się w komórkę T pomocniczą Th262.

Atopowe zapalenie skóry

Patogeneza atopowego zapalenia skóry (AZS) odzwierciedla się głównie poprzez złożoną interakcję między dysfunkcją bariery naskórkowej, nieprawidłową mikrobiotą skóry i dysregulowaną odpornością komórek T typu 263. Pacjenci z atopowym zapaleniem skóry związanym z wadliwą filagryną (białko strukturalne w warstwie rogowej naskórka) mają wysokie ryzyko rozwinięcia również alergicznego kontaktowego zapalenia skóry64.

Cetyryzyna okazała się skuteczna w zmniejszaniu świądu u pacjentów z AZS poprzez hamowanie świądu wywołanego histaminą i zmniejszenie markerów zapalnych, takich jak IL-4 i IL-1365.

Alergia pokarmowa

Alergia pokarmowa (FA) to zależna od IgE nadwrażliwość typu I na określony alergen pokarmowy66. Jej proces patologiczny jest podzielony na dwa etapy: w fazie sensytyzacji alergicznej początkowa ekspozycja na alergen prowadzi do załamania tolerancji, z następującym wytwarzaniem specyficznego IgE, substancji wazoaktywnych i mediatorów odpowiedzi alergicznej, takich jak histamina i czynnik aktywujący płytki67.

Układ odpornościowy zwykle rozwija tolerancję na białka pokarmowe, przynajmniej częściowo dzięki działaniu regulatorowych limfocytów T CD4+68. Alergia pokarmowa rozwija się, gdy układ odpornościowy montuje odpowiedź mediowaną przez komórki T pomocnicze 2 (TH2) przeciwko epitopom pokarmowym. Sensytyzacja TH2 może początkowo występować na skórze, a nie w przewodzie pokarmowym69.

Pacjenci z ustaloną alergią pokarmową mogą zostać odczuleni na alergeny pokarmowe poprzez immunoterapię doustną, która według przypuszczeń obejmuje przesunięcie od specyficznych dla alergenu komórek TH2 do regulatorowych limfocytów T CD4+, komórek anergicznych i apoptotycznych70.

Implikacje dla interwencji terapeutycznych

Leki przeciwhistaminowe

Leki przeciwhistaminowe są klasą leków powszechnie stosowanych w leczeniu objawów alergii, takich jak katar, kichanie i swędzące oczy71. Działają one poprzez blokowanie receptorów histaminowych72. Histamina jest chemiczną substancją uwalnianą przez układ odpornościowy w celu przekazywania wiadomości między różnymi komórkami. Ma ona kilka funkcji, ale jest głównie znana ze swojej roli w wywoływaniu objawów alergicznych i anafilaktycznych73.

Cetyryzyna, lek przeciwhistaminowy drugiej generacji, ma dobrze ustalony profil bezpieczeństwa, szczególnie w przypadku długotrwałego stosowania, i utrzymuje swoją skuteczność w czasie74. Brak znaczących efektów sedatywnych pozwala pacjentom na utrzymanie normalnej aktywności i produktywności, co zwiększa przestrzeganie zaleceń leczenia i ogólne zadowolenie75.

Leki przeciwzapalne

Kortykosteroidy i inne leki immunosupresyjne są stosowane w leczeniu chorób alergicznych76. Kortykosteroidy donosowe (INS), często stosowane jako leczenie pierwszego rzutu u pacjentów z łagodnymi przetrwałymi lub umiarkowanymi do ciężkich objawami, działają miejscowo w błonie śluzowej nosa, blokując wiele mediatorów zaangażowanych w kaskadę alergiczną, w tym histaminę, cytokiny, leukotrieny, chemokiny, prostaglandyny i tryptazę77.

Modyfikatory leukotrienów

Montelukast pomaga poprawić objawy astmy poprzez blokowanie substancji w organizmie zwanych leukotrienami, które powodują stan zapalny78. Jest również stosowany do kontrolowania objawów alergii, takich jak kichanie, zatkany, cieknący i swędzący nos79.

Terapie biologiczne

Omalizumab (który blokuje wiązanie IgE do jego receptorów) zmniejsza reaktywność komórek tucznych i wrażliwość na aktywację, co może zmniejszyć epizody anafilaksji80.

Fasenra (benralizumab) jest lekiem zaprojektowanym do zwalczania i usuwania eozynofilów, kluczowej przyczyny astmy81. Mechanizm działania Fasenry w astmie nie jest w pełni zrozumiały, ale lek ten pomaga zapobiegać atakom astmy i może poprawić oddychanie poprzez zmniejszenie poziomu eozynofilów we krwi82.

Immunoterapia

Immunoterapia alergenowa (AIT), lub odczulanie, polega na podawaniu określonego alergenu w stopniowo zwiększających się dawkach, ostatecznie rozwijając odporność lub tolerancję na alergen83. Podczas AIT odpowiedź układu odpornościowego ulega zmianie. Te zmiany mogą obejmować produkcję mniejszej ilości IgE, produkcję „blokujących” przeciwciał IgG oraz produkcję większej liczby regulatorowych limfocytów T, promujących tolerancję i mniej aktywną odpowiedź immunologiczną84.

Badania nad nowymi celami terapeutycznymi, takimi jak szlak sygnałowy IL-3, mogą prowadzić do nowych opcji leczenia i zapobiegania reakcjom alergicznym, w tym świądowi85.

Nowe odkrycia w patogenezie alergii

Badania nad alergią skupiają się coraz bardziej na połączeniu wrodzonego i adaptacyjnego układu odpornościowego w patogenezie choroby86. Powierzchnia oka wykazuje obecność receptorów rozpoznających patogeny, kluczowego elementu w rozpoznawaniu produktów mikrobiologicznych, na które wszyscy jesteśmy narażeni87.

Naukowcy zidentyfikowali niedawno specyficzny typ komórek immunologicznych w skórze, nazwany komórkami GD3, które produkują cząsteczkę zwaną IL-3 w odpowiedzi na czynniki środowiskowe, w tym mikroby, które normalnie żyją na skórze88. IL-3 działa bezpośrednio na podzbiór neuronów czuciowych wywołujących świąd, zwiększając ich reaktywność nawet na niskie poziomy alergenów proteazowych z powszechnych źródeł, takich jak roztocza kurzu domowego, pleśnie środowiskowe i komary89.

Badacze odkryli również mechanizm, za pomocą którego cząsteczka stworzona przez człowieka (DARPin E2-79) niszczy kompleksy indukujące reakcje alergiczne poprzez oddzielanie przeciwciała IgE od jego partnera, cząsteczki zwanej FcεR90. To odkrycie mogłoby prowadzić do interwencji przeciwko szerokiemu spektrum ostrych reakcji alergicznych91.

Inne badania wskazują na rolę komórek jelitowych w tolerancji pokarmowej i alergiach. Nowe badania identyfikują specyficzne typy komórek jelitowych, które komunikują się z limfocytami T, skłaniając je do tolerowania, atakowania lub po prostu ignorowania, i wyjaśniają, jak te przeciwstawne odpowiedzi są wyzwalane92. Te odkrycia dają naukowcom nowe zrozumienie tego, jak jelitowy układ odpornościowy utrzymuje jelito w równowadze i mogą ostatecznie rzucić światło na podstawowe przyczyny i mechanizmy alergii pokarmowych93.

Podsumowanie

Patogeneza chorób alergicznych jest złożona i obejmuje wiele czynników, w tym predyspozycje genetyczne, ekspozycję środowiskową, mikrobiotę jelitową oraz stan układu odpornościowego9495. Głównym mechanizmem jest nieprawidłowa odpowiedź układu odpornościowego, w której komórki TH2 i przeciwciała IgE odgrywają kluczową rolę96.

Reakcja alergiczna obejmuje fazę wczesną, charakteryzującą się degranulacją komórek tucznych i uwolnieniem mediatorów zapalnych, oraz fazę późną, związaną z rekrutacją komórek zapalnych i przewlekłym stanem zapalnym97. Heterogenność patogenezy chorób alergicznych prowadzi do różnych fenotypów klinicznych, w tym alergicznego nieżytu nosa, astmy alergicznej, atopowego zapalenia skóry i alergii pokarmowej98.

Zrozumienie patofizjologii chorób alergicznych jest kluczowe dla opracowania nowych strategii terapeutycznych99. Nowe odkrycia w dziedzinie immunologii alergii otwierają drogę do bardziej ukierunkowanych i skutecznych interwencji terapeutycznych, które mogą poprawić jakość życia pacjentów z chorobami alergicznymi100.

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  1. 09.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Pathogenesis of allergic diseases and implications for therapeutic interventions | Signal Transduction and Targeted Therapy
    https://www.nature.com/articles/s41392-023-01344-4
    Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. […] The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. […] The pathogenesis of AD is mainly reflected by a complex interplay between epidermal barrier dysfunction, abnormal skin microbiota and dysregulated type 2 T cell immunity. […] FA is an IgE-dependent type I hypersensitivity to a specific food allergen.
  • #2 Pathogenesis of allergic diseases and implications for therapeutic interventions
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10039055/
    Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. The pathogenesis of AD is mainly reflected by a complex interplay between epidermal barrier dysfunction, abnormal skin microbiota and dysregulated type 2 T cell immunity. FA is an IgE-dependent type I hypersensitivity to a specific food allergen. Its pathological process is divided into two stages: in the allergic sensitization stage, the initial exposure to the allergen results in tolerance breakdown, with subsequent generation of specific IgE, vasoactive substances and allergic response mediators such as histamine and platelet activating factor. The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function.
  • #3 Pathogenesis of allergic diseases and implications for therapeutic interventions | Signal Transduction and Targeted Therapy
    https://www.nature.com/articles/s41392-023-01344-4
    The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function. […] The immunopathological profiles of AR and AAS are very similar in terms of eosinophil, mast cell and Th2 cell infiltration. […] In the AAS disease, mucosal pathological alterations comprise epithelial hyperplasia, goblet cell metaplasia and increased mucus generation. […] Allergens cross-link IgE that interact with mast cells, which further induces the release of multiple mediators (including histamine and leukotrienes), promotes arteriole dilation and vascular permeability, and causes pruritus, runny nose, mucus secretion, and pulmonary smooth muscle contraction. […] The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function.
  • #4 Pathogenesis of allergic diseases and implications for therapeutic interventions
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10039055/
    The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively.
  • #5 Allergic Reactions
    https://www.aaaai.org/tools-for-the-public/conditions-library/allergies/allergic-reactions
    Allergic reactions are actually a result of a chain reaction that begins in your genes and is expressed by your immune system. […] Your immune system identifies pollen as an invader or allergen. Your immune system overreacts by producing antibodies called Immunoglobulin E (IgE). These antibodies travel to cells that release chemicals, causing an allergic reaction. […] It is not yet fully understood why some substances trigger allergies and others do not, nor why some people have allergic reactions while others do not. […] A family history of allergies is the single most important factor that puts you at risk of developing allergic disease. […] Allergy symptoms are the result of a chain reaction that starts in your immune system. […] If you have a family history of allergies, you are at a much higher risk of developing allergic disease.
  • #6 Allergies explained | Better Health Channel
    https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/allergies
    The immune systems tendency to overreact to a harmless substance is thought to be genetic. The term atopy describes this genetic tendency. Doctors and clinical immunology/allergy specialists describe a person who has an allergy as being atopic such people usually have raised levels of IgE in their blood.
  • #7 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    Allergic reactions are triggered when allergens cross-link preformed IgE bound to the high-affinity receptor FcRI on mast cells. Mast cells line the body surfaces and serve to alert the immune system to local infection. Once activated, they induce inflammatory reactions by secreting chemical mediators stored in preformed granules, and by synthesizing leukotrienes and cytokines after activation occurs. […] The immediate allergic reaction caused by mast-cell degranulation is followed by a more sustained inflammation, known as the late-phase response. This late response involves the recruitment of other effector cells, notably TH2 lymphocytes, eosinophils, and basophils, which contribute significantly to the immunopathology of an allergic response. […] Most antibodies are found in body fluids and engage effector cells, through receptors specific for the Fc constant regions, only after binding specific antigen through the antibody variable regions. IgE, however, is an exception as it is captured by the high-affinity Fc receptor in the absence of bound antigen.
  • #8 Allergy – Wikipedia
    https://en.wikipedia.org/wiki/Allergy
    Allergies, also known as allergic diseases, are various conditions caused by hypersensitivity of the immune system to typically harmless substances in the environment. These diseases include hay fever, food allergies, atopic dermatitis, allergic asthma, and anaphylaxis. Symptoms may include red eyes, an itchy rash, sneezing, coughing, a runny nose, shortness of breath, or swelling. […] The underlying mechanism involves immunoglobulin E antibodies (IgE), part of the body’s immune system, binding to an allergen and then to a receptor on mast cells or basophils where it triggers the release of inflammatory chemicals such as histamine. […] In the initial stages of allergy, a type I hypersensitivity reaction against an allergen encountered for the first time and presented by a professional antigen-presenting cell causes a response in a type of immune cell called a TH2 lymphocyte, a subset of T cells that produce a cytokine called interleukin-4 (IL-4).
  • #9 The Pathogenesis of Allergy: A Brief Introduction | SpringerLink
    https://link.springer.com/chapter/10.1007/978-94-017-7444-4_3
    Allergic diseases are mainly IgE-mediated diseases that include allergic rhinitis, allergic asthma, allergic dermatitis, and food allergy, etc. […] It has been proposed that some people are genetically prone to develop allergic diseases. […] When these people encounter foreign antigens, dendritic cells capture and process the antigens, transfer the antigen information to T helper (TH) cells, and a skewed immune response is induced that results in a TH2 polarization status in the body. […] These antigen-specific TH2 cells present the antigen information to B cells and drive these cells to become plasma cells that produce antigen-specific IgE. […] This antigen-specific IgE sensitizes mast cells by binding to the high-affinity IgE receptors on their surface. […] When the sensitized mast cells are re-exposed to the specific antigens, they are activated to release allergic mediators such as histamine, tryptase, leukotrines, and serotonin, etc. that initiate allergic attacks.
  • #10 The Pathogenesis of Allergy: A Brief Introduction | SpringerLink
    https://link.springer.com/chapter/10.1007/978-94-017-7444-4_3
    Allergic diseases are mainly IgE-mediated diseases that include allergic rhinitis, allergic asthma, allergic dermatitis, and food allergy, etc. […] It has been proposed that some people are genetically prone to develop allergic diseases. […] When these people encounter foreign antigens, dendritic cells capture and process the antigens, transfer the antigen information to T helper (TH) cells, and a skewed immune response is induced that results in a TH2 polarization status in the body. […] These antigen-specific TH2 cells present the antigen information to B cells and drive these cells to become plasma cells that produce antigen-specific IgE. […] This antigen-specific IgE sensitizes mast cells by binding to the high-affinity IgE receptors on their surface. […] When the sensitized mast cells are re-exposed to the specific antigens, they are activated to release allergic mediators such as histamine, tryptase, leukotrines, and serotonin, etc. that initiate allergic attacks.
  • #11 Allergy | British Society for Immunology
    https://www.immunology.org/policy-and-public-affairs/briefings-and-position-statements/allergy
    An allergy is an unnecessary immune response to an innocuous substance. […] Allergies can range in severity from symptoms of mild discomfort to the life-threatening systemic reaction seen in anaphylaxis. […] The process through which a person’s body becomes sensitive to a given allergen is known as sensitisation. […] When allergens enter the body, antigen presenting cells (immune cells that capture incoming substances and present them to other immune cells, initiating a cascade of immune responses) at body surfaces, capture and present them to immune cells, particularly T cells. […] Through a number of immune interactions between T cells and B cells, B cells produce allergen-specific IgE antibodies. […] Mast cells are granular cells, meaning they contain many secretory granules which, when activated, release their contents into the blood stream.
  • #12 Combattre les allergies – L’actu de l’Institut Pasteur
    https://www.pasteur.fr/en/home/research-journal/reports/tackling-allergies
    They disrupt the lives of millions of people in France and can have extremely serious complications. Allergies are caused by a deregulation of the immune system, which „overreacts” to substances in the environment known as „allergens”. […] Allergies occur most often in those with a genetic predisposition, with one or more allergy sufferers among their family members. Individuals with allergies have a form of hypersensitivity; they suffer from a pathological exaggeration of the immune response, especially the inflammatory reaction, when they inhale, swallow or touch an allergen. […] A few days after the body first comes into contact with an allergen, it produces specific antibodies to protect against it, known as IgE (immunoglobulin E) antibodies, which bind to the surface of mast cells. This first stage, known as „sensitization”, does not give rise to any symptoms.
  • #13 The Pathogenesis of Allergy: A Brief Introduction | SpringerLink
    https://link.springer.com/chapter/10.1007/978-94-017-7444-4_3
    Allergic diseases are mainly IgE-mediated diseases that include allergic rhinitis, allergic asthma, allergic dermatitis, and food allergy, etc. […] It has been proposed that some people are genetically prone to develop allergic diseases. […] When these people encounter foreign antigens, dendritic cells capture and process the antigens, transfer the antigen information to T helper (TH) cells, and a skewed immune response is induced that results in a TH2 polarization status in the body. […] These antigen-specific TH2 cells present the antigen information to B cells and drive these cells to become plasma cells that produce antigen-specific IgE. […] This antigen-specific IgE sensitizes mast cells by binding to the high-affinity IgE receptors on their surface. […] When the sensitized mast cells are re-exposed to the specific antigens, they are activated to release allergic mediators such as histamine, tryptase, leukotrines, and serotonin, etc. that initiate allergic attacks.
  • #14 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    The inflammatory response after IgE-mediated mast-cell activation occurs as an immediate reaction, starting within seconds, and a late reaction, which takes up to 812 hours to develop. […] The late-phase reaction is an important cause of much serious long-term illness, as for example in chronic asthma. […] The allergic response to innocuous antigens reflects the pathophysiological aspects of a defensive immune response whose physiological role is to protect against helminthic parasites. It is triggered by antigen binding to IgE antibodies bound to the high-affinity IgE receptor FcRI on mast cells. […] The resulting inflammation can be divided into early events, characterized by short-lived mediators such as histamine, and later events that involve leukotrienes, cytokines, and chemokines, which recruit and activate eosinophils and basophils. The late phase of this response can evolve into chronic inflammation, characterized by the presence of effector T cells and eosinophils, which is most clearly seen in chronic allergic asthma.
  • #15 Allergy – Wikipedia
    https://en.wikipedia.org/wiki/Allergy
    Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth muscle contraction. […] After the chemical mediators of the acute response subside, late-phase responses can often occur. This is due to the migration of other leukocytes such as neutrophils, lymphocytes, eosinophils, and macrophages to the initial site. […] Allergic contact dermatitis is termed an „allergic” reaction (which usually refers to type I hypersensitivity), its pathophysiology involves a reaction that more correctly corresponds to a type IV hypersensitivity reaction.
  • #16 MedlinePlus: Histamine: The Stuff Allergies are Made ofLock
    https://medlineplus.gov/medlineplus-videos/histamine-the-stuff-allergies-are-made-of/
    Histamine plays a big role in all of them. […] Histamine is a signaling molecule, sending messages between cells. […] Histamine also works with our immune system. […] When the immune system discovers an invader, immune cells called B-cells make IgE antibodies. […] Eventually mast cells and basophils pick up the IgE’s and become sensitized. […] When they come in contact with a target invader…They spew histamine and other inflammatory chemicals. […] But with allergies, the immune system overreacts to harmless substances, not parasites. This is when histamine becomes our foe. […] Leaky vessels cause tearing in eyes, congestion in the nose, and swelling…basically anywhere. […] Most worrisome is when histamine causes anaphylaxis, a severe reaction that is potentially fatal. […] Antihistamines block cells from seeing histamine and can treat common allergies.
  • #17 A Review on Mechanism of Histamine Mediated Allergic Reactions: Therapeutic Role, Safety, and Clinical Efficacy of Cetirizine in Modern Allergy and Other Diseases Management – Biomedical and Pharmacology Journal
    https://biomedpharmajournal.org/vol18no1/a-review-on-mechanism-of-histamine-mediated-allergic-reactions-therapeutic-role-safety-and-clinical-efficacy-of-cetirizine-in-modern-allergy-and-other-diseases-management/
    Upon binding to the H1 receptor, histamine triggers a cascade involving Gq/11 protein activation and phospholipase C signaling, producing DAG and IP3. This promotes smooth muscle contraction, increases vascular permeability, as well as contributes to the hallmark symptoms of allergic responses, such as itchiness, bronchoconstriction, and tissue swelling. […] Histamine release is one of the primary consequences of mast cell activation, which causes an immediate allergic reaction. […] The mechanism by which mast cells release histamine in response to an antigen-antibody reaction. […] Histamine is produced and released by various human cells, including lymphocytes, enterochromaffin cells, basophils, mast cells, platelets, and histaminergic neurons. […] Histamine has various physiological and pathophysiological effects on histamine receptors.
  • #18 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    The inflammatory response after IgE-mediated mast-cell activation occurs as an immediate reaction, starting within seconds, and a late reaction, which takes up to 812 hours to develop. […] The late-phase reaction is an important cause of much serious long-term illness, as for example in chronic asthma. […] The allergic response to innocuous antigens reflects the pathophysiological aspects of a defensive immune response whose physiological role is to protect against helminthic parasites. It is triggered by antigen binding to IgE antibodies bound to the high-affinity IgE receptor FcRI on mast cells. […] The resulting inflammation can be divided into early events, characterized by short-lived mediators such as histamine, and later events that involve leukotrienes, cytokines, and chemokines, which recruit and activate eosinophils and basophils. The late phase of this response can evolve into chronic inflammation, characterized by the presence of effector T cells and eosinophils, which is most clearly seen in chronic allergic asthma.
  • #19 Allergy – Wikipedia
    https://en.wikipedia.org/wiki/Allergy
    Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth muscle contraction. […] After the chemical mediators of the acute response subside, late-phase responses can often occur. This is due to the migration of other leukocytes such as neutrophils, lymphocytes, eosinophils, and macrophages to the initial site. […] Allergic contact dermatitis is termed an „allergic” reaction (which usually refers to type I hypersensitivity), its pathophysiology involves a reaction that more correctly corresponds to a type IV hypersensitivity reaction.
  • #20 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    Allergic reactions are triggered when allergens cross-link preformed IgE bound to the high-affinity receptor FcRI on mast cells. Mast cells line the body surfaces and serve to alert the immune system to local infection. Once activated, they induce inflammatory reactions by secreting chemical mediators stored in preformed granules, and by synthesizing leukotrienes and cytokines after activation occurs. […] The immediate allergic reaction caused by mast-cell degranulation is followed by a more sustained inflammation, known as the late-phase response. This late response involves the recruitment of other effector cells, notably TH2 lymphocytes, eosinophils, and basophils, which contribute significantly to the immunopathology of an allergic response. […] Most antibodies are found in body fluids and engage effector cells, through receptors specific for the Fc constant regions, only after binding specific antigen through the antibody variable regions. IgE, however, is an exception as it is captured by the high-affinity Fc receptor in the absence of bound antigen.
  • #21 The pathophysiology of allergic responses | Nursing Times
    https://www.nursingtimes.net/respiratory/the-pathophysiology-of-allergic-responses-16-05-2006/
    These include largely histamine and other mediators, including cysteinyl leukotrienes, prostaglandins and kinins. […] The early asthmatic response After allergen exposure, inflammatory mediators, including large quantities of histamine, are released from mast cells on the mucosal surfaces. […] Cysteinyl leukotrienes, also released from mast cells, are also potent bronchoconstrictors of airway smooth muscle, amplifying the action of histamine. […] A characteristic of the late-phase asthmatic response is the infiltration of the airways with inflammatory cells and mediators, in particular eosinophils, which results in airway narrowing and associated bronchial hyper-responsiveness. […] Eosinophils play an important role in the pathophysiology of asthma, and their migration into the lungs is associated with inflammation and bronchoconstriction.
  • #22 The pathophysiology of allergic responses | Nursing Times
    https://www.nursingtimes.net/respiratory/the-pathophysiology-of-allergic-responses-16-05-2006/
    These include largely histamine and other mediators, including cysteinyl leukotrienes, prostaglandins and kinins. […] The early asthmatic response After allergen exposure, inflammatory mediators, including large quantities of histamine, are released from mast cells on the mucosal surfaces. […] Cysteinyl leukotrienes, also released from mast cells, are also potent bronchoconstrictors of airway smooth muscle, amplifying the action of histamine. […] A characteristic of the late-phase asthmatic response is the infiltration of the airways with inflammatory cells and mediators, in particular eosinophils, which results in airway narrowing and associated bronchial hyper-responsiveness. […] Eosinophils play an important role in the pathophysiology of asthma, and their migration into the lungs is associated with inflammation and bronchoconstriction.
  • #23 The pathophysiology of allergic responses | Nursing Times
    https://www.nursingtimes.net/respiratory/the-pathophysiology-of-allergic-responses-16-05-2006/
    The early-phase reaction After sensitisation to an allergen has occurred, and on subsequent re-exposure, cross-linking of allergen on IgE displayed on the surfaces of mast cells in the nasal mucosa causes degranulation. […] The late-phase reaction After the early response in the nose following allergen exposure, inflammatory cells continue to be recruited. […] As with the asthmatic late response, eosinophils play an important role in the late-phase response in the nose, with the enzymes and proteins released causing tissue damage and further inflammation. […] An understanding of the pathophysiology of allergic disease is crucial in assisting in the management of allergic disease and symptoms.
  • #24 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    The inflammatory response after IgE-mediated mast-cell activation occurs as an immediate reaction, starting within seconds, and a late reaction, which takes up to 812 hours to develop. […] The late-phase reaction is an important cause of much serious long-term illness, as for example in chronic asthma. […] The allergic response to innocuous antigens reflects the pathophysiological aspects of a defensive immune response whose physiological role is to protect against helminthic parasites. It is triggered by antigen binding to IgE antibodies bound to the high-affinity IgE receptor FcRI on mast cells. […] The resulting inflammation can be divided into early events, characterized by short-lived mediators such as histamine, and later events that involve leukotrienes, cytokines, and chemokines, which recruit and activate eosinophils and basophils. The late phase of this response can evolve into chronic inflammation, characterized by the presence of effector T cells and eosinophils, which is most clearly seen in chronic allergic asthma.
  • #25 Allergy | British Society for Immunology
    https://www.immunology.org/policy-and-public-affairs/briefings-and-position-statements/allergy
    An allergy is an unnecessary immune response to an innocuous substance. […] Allergies can range in severity from symptoms of mild discomfort to the life-threatening systemic reaction seen in anaphylaxis. […] The process through which a person’s body becomes sensitive to a given allergen is known as sensitisation. […] When allergens enter the body, antigen presenting cells (immune cells that capture incoming substances and present them to other immune cells, initiating a cascade of immune responses) at body surfaces, capture and present them to immune cells, particularly T cells. […] Through a number of immune interactions between T cells and B cells, B cells produce allergen-specific IgE antibodies. […] Mast cells are granular cells, meaning they contain many secretory granules which, when activated, release their contents into the blood stream.
  • #26 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    Allergic reactions are triggered when allergens cross-link preformed IgE bound to the high-affinity receptor FcRI on mast cells. Mast cells line the body surfaces and serve to alert the immune system to local infection. Once activated, they induce inflammatory reactions by secreting chemical mediators stored in preformed granules, and by synthesizing leukotrienes and cytokines after activation occurs. […] The immediate allergic reaction caused by mast-cell degranulation is followed by a more sustained inflammation, known as the late-phase response. This late response involves the recruitment of other effector cells, notably TH2 lymphocytes, eosinophils, and basophils, which contribute significantly to the immunopathology of an allergic response. […] Most antibodies are found in body fluids and engage effector cells, through receptors specific for the Fc constant regions, only after binding specific antigen through the antibody variable regions. IgE, however, is an exception as it is captured by the high-affinity Fc receptor in the absence of bound antigen.
  • #27 Allergy | British Society for Immunology
    https://www.immunology.org/policy-and-public-affairs/briefings-and-position-statements/allergy
    In the case of allergy, binding of an allergen to IgE-mast cells results in their rapid degranulation and the release of inflammatory compounds, including histamine, which contribute to local inflammation and the symptoms associated with allergy. […] Allergy is widespread in the UK and worldwide and the number of people affected and experiencing severe allergic symptoms continues to increase, particularly in the developed world. […] The idea that exposure to infectious agents may decrease the risk of allergy was first introduced in 1989. […] One of these is the skewing towards an immune profile of T helper 2 cells (Th2 cells) over T helper 1 cells. […] Allergy immunotherapy (AIT), or desensitisation involves administration of a particular allergen, given in gradually increasing doses, eventually developing immunity or tolerance to the allergen.
  • #28 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    The ligation of cell-bound IgE antibody by specific antigen triggers activation of these cells at the site of antigen entry into the tissues. The release of inflammatory lipid mediators, cytokines, and chemokines at sites of IgE-triggered reactions results in the recruitment of eosinophils and basophils to augment the type I response. […] Mast cells express FcRI constitutively on their surface and are activated when antigens cross-link IgE bound to these receptors. Degranulation occurs within seconds, releasing a variety of preformed inflammatory mediators. […] On activation, mast cells synthesize and release chemokines, lipid mediators such as leukotrienes and platelet-activating factor (PAF), and additional cytokines such as IL-4 and IL-13 which perpetuate the TH2 response. These mediators contribute to both the acute and the chronic inflammatory responses.
  • #29 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    IgE-mediated activation of mast cells thus orchestrates an important inflammatory cascade that is amplified by the recruitment of eosinophils, basophils, and TH2 lymphocytes. […] Eosinophils are granulocytic leukocytes that originate in bone marrow. […] Eosinophils have two kinds of effector function. First, on activation they release highly toxic granule proteins and free radicals, which can kill microorganisms and parasites but can also cause significant tissue damage in allergic reactions. […] The activation and degranulation of eosinophils is strictly regulated, as their inappropriate activation would be very harmful to the host. […] In a local allergic reaction, mast-cell degranulation and TH2 activation cause eosinophils to accumulate in large numbers and to become activated. Their continued presence is characteristic of chronic allergic inflammation and they are thought to be major contributors to tissue damage.
  • #30 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    IgE-mediated activation of mast cells thus orchestrates an important inflammatory cascade that is amplified by the recruitment of eosinophils, basophils, and TH2 lymphocytes. […] Eosinophils are granulocytic leukocytes that originate in bone marrow. […] Eosinophils have two kinds of effector function. First, on activation they release highly toxic granule proteins and free radicals, which can kill microorganisms and parasites but can also cause significant tissue damage in allergic reactions. […] The activation and degranulation of eosinophils is strictly regulated, as their inappropriate activation would be very harmful to the host. […] In a local allergic reaction, mast-cell degranulation and TH2 activation cause eosinophils to accumulate in large numbers and to become activated. Their continued presence is characteristic of chronic allergic inflammation and they are thought to be major contributors to tissue damage.
  • #31 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    IgE-mediated activation of mast cells thus orchestrates an important inflammatory cascade that is amplified by the recruitment of eosinophils, basophils, and TH2 lymphocytes. […] Eosinophils are granulocytic leukocytes that originate in bone marrow. […] Eosinophils have two kinds of effector function. First, on activation they release highly toxic granule proteins and free radicals, which can kill microorganisms and parasites but can also cause significant tissue damage in allergic reactions. […] The activation and degranulation of eosinophils is strictly regulated, as their inappropriate activation would be very harmful to the host. […] In a local allergic reaction, mast-cell degranulation and TH2 activation cause eosinophils to accumulate in large numbers and to become activated. Their continued presence is characteristic of chronic allergic inflammation and they are thought to be major contributors to tissue damage.
  • #32 The pathophysiology of allergic responses | Nursing Times
    https://www.nursingtimes.net/respiratory/the-pathophysiology-of-allergic-responses-16-05-2006/
    Allergy is the clinical expression of atopy – the physical symptoms of allergy related to exposure. […] The immune response is dependent on the bodys two subsets of T-lymphocytes, known as T helper cells TH1 and TH2. […] In atopic individuals, TH2 cells and their mediators encourage the immune system to recognise allergens as an invader, and mount a response against them. […] For allergy to exist, allergen sensitisation must first occur. […] The antigen-presenting cells come into contact with the allergen which, in people predisposed to atopy, is perceived to be an invader. […] After the period of sensitisation described above there is a period of latency, and on subsequent re-exposure to the allergen the allergic response is triggered: allergen cross-links with the IgE on the surfaces of the mast cell or basophil, causing the cell to degranulate or release inflammatory mediators.
  • #33 The pathophysiology of allergic responses | Nursing Times
    https://www.nursingtimes.net/respiratory/the-pathophysiology-of-allergic-responses-16-05-2006/
    Allergy is the clinical expression of atopy – the physical symptoms of allergy related to exposure. […] The immune response is dependent on the bodys two subsets of T-lymphocytes, known as T helper cells TH1 and TH2. […] In atopic individuals, TH2 cells and their mediators encourage the immune system to recognise allergens as an invader, and mount a response against them. […] For allergy to exist, allergen sensitisation must first occur. […] The antigen-presenting cells come into contact with the allergen which, in people predisposed to atopy, is perceived to be an invader. […] After the period of sensitisation described above there is a period of latency, and on subsequent re-exposure to the allergen the allergic response is triggered: allergen cross-links with the IgE on the surfaces of the mast cell or basophil, causing the cell to degranulate or release inflammatory mediators.
  • #34 Allergic rhinitis – Wikipedia
    https://en.wikipedia.org/wiki/Allergic_rhinitis
    Allergic rhinitis, of which the seasonal type is called hay fever, is a type of inflammation in the nose that occurs when the immune system overreacts to allergens in the air. It is classified as a type I hypersensitivity reaction. […] The underlying mechanism involves IgE antibodies that attach to an allergen, and subsequently result in the release of inflammatory chemicals such as histamine from mast cells. […] The pathophysiology of allergic rhinitis involves Th2 Helper T cell and IgE mediated inflammation with overactive function of the adaptive and innate immune systems. The process begins when an aeroallergen penetrates the nasal mucosal barrier. […] The allergen is then engulfed by an antigen presenting cell (APC) (such as a dendritic cell). The APC then presents the antigen to a Naive CD4+ helper T cell stimulating it to differentiate into a Th2 helper T cell. The Th2 helper T cell then secretes inflammatory cytokines including IL-4, IL-5, IL-13, IL-14, and IL-31.
  • #35 Allergic Diseases: A Comprehensive Review on Risk Factors, Immunological Mechanisms, Link with COVID-19, Potential Treatments, and Role of Allergen Bioinformatics
    https://www.mdpi.com/1660-4601/18/22/12105
    They regulate the activation and recruitment of pro-inflammatory cells (mast cells and eosinophils) in mucosal target organs, as well as the class switching of IgE in B cells. […] Allergy symptoms and inflammation are triggered by these activations. […] The microbiota (intestinal microflora) are a collection of microorganisms, primarily bacteria, that form a complex ecosystem in the human digestive tract. […] The gut microbiota plays a significant role in the formation of immune system organs and help to identify host immune response patterns. […] Dysbiosis is described as a disruption in gut homeostasis caused by a change in the function and composition of the microbiota. […] Numerous studies suggest that dysbiosis intestinal, or quantitative and qualitative abnormalities in the microflora composition, may be a factor in the pathogenesis of a variety of disorders, including allergic disorders.
  • #36 Allergic Cascade: Mechanism of Reaction & Early vs. Late Phase
    https://www.medicinenet.com/allergic_cascade/article.htm
    The allergic cascade refers to allergic reactions that happen in the body in response to allergens. A variety of immune cells and chemical messengers participate in the allergic cascade. Symptoms of the allergic cascade range from mild swelling and itching to full-blown anaphylactic shock. […] The end result is a well-defined constellation of signs and symptoms produced by the „allergic cascade.” […] Cytokines are a diverse group of proteins that are released by lymphocytes and macrophages in response to an injury or activation, such as by an allergen. They act as chemical signals that „step up” or „step down” the immune reaction. […] The balance between allergy-promoting TH2 cells and infection-fighting TH1 cells has been found to be a critical component of our immune system. […] The late phase reaction involves an influx of a variety of inflammatory cells (eosinophils, neutrophils, lymphocytes, and mast cells) to the affected area, and if repeated inhalations of allergens cause recurrent reactions, these reactions may merge into each other leading to chronic or persistent allergic asthma. […] By looking closely at the complex steps involved in this chain of events, scientists have been able to find new and innovative treatments for common and troublesome allergic illnesses.
  • #37 Allergic Diseases: A Comprehensive Review on Risk Factors, Immunological Mechanisms, Link with COVID-19, Potential Treatments, and Role of Allergen Bioinformatics
    https://www.mdpi.com/1660-4601/18/22/12105
    An allergic IgE mediated mechanism was later discovered to disproportionately activate specific immune system cells and to release inflammatory mediators. […] The role of the immune system is to protect the body against invading pathogens causing different diseases. When the immune system misidentifies a harmless foreign antigen as a pathogen, an allergic reaction occurs. […] In genetically predisposed individuals, an imbalance in the immune system’s regulatory mechanisms may lead to allergic diseases or autoimmune disorders, depending on the nature of the antigen. […] During an allergic reaction, the immune system must detect pathogenic stimuli and generate a robust immune response. […] Specific antigen sensitization is required for allergic diseases development. Inflammatory cytokines (IL-13, IL-4, and IL-5) are produced as a result of cell expansion and differentiation to T2 cell subtypes.
  • #38 Types of Allergies – Global Allergy & Airways Patient PlatformExpandExpandExpandExpandExpandExpandToggle MenuScroll to topScroll to topExpandExpandExpandExpandExpandExpand
    https://gaapp.org/diseases/allergies/types-of-allergies
    These observations suggest that IgE is instrumental in the immune system’s response to allergens by virtue of its ability to trigger mast cell mediator release, leading directly to both the early and late phase reactions. […] Histamine is stored within the mast cell and released during the allergic reaction.
  • #39 A Review on Mechanism of Histamine Mediated Allergic Reactions: Therapeutic Role, Safety, and Clinical Efficacy of Cetirizine in Modern Allergy and Other Diseases Management – Biomedical and Pharmacology Journal
    https://biomedpharmajournal.org/vol18no1/a-review-on-mechanism-of-histamine-mediated-allergic-reactions-therapeutic-role-safety-and-clinical-efficacy-of-cetirizine-in-modern-allergy-and-other-diseases-management/
    Upon binding to the H1 receptor, histamine triggers a cascade involving Gq/11 protein activation and phospholipase C signaling, producing DAG and IP3. This promotes smooth muscle contraction, increases vascular permeability, as well as contributes to the hallmark symptoms of allergic responses, such as itchiness, bronchoconstriction, and tissue swelling. […] Histamine release is one of the primary consequences of mast cell activation, which causes an immediate allergic reaction. […] The mechanism by which mast cells release histamine in response to an antigen-antibody reaction. […] Histamine is produced and released by various human cells, including lymphocytes, enterochromaffin cells, basophils, mast cells, platelets, and histaminergic neurons. […] Histamine has various physiological and pathophysiological effects on histamine receptors.
  • #40 The pathophysiology of allergic responses | Nursing Times
    https://www.nursingtimes.net/respiratory/the-pathophysiology-of-allergic-responses-16-05-2006/
    These include largely histamine and other mediators, including cysteinyl leukotrienes, prostaglandins and kinins. […] The early asthmatic response After allergen exposure, inflammatory mediators, including large quantities of histamine, are released from mast cells on the mucosal surfaces. […] Cysteinyl leukotrienes, also released from mast cells, are also potent bronchoconstrictors of airway smooth muscle, amplifying the action of histamine. […] A characteristic of the late-phase asthmatic response is the infiltration of the airways with inflammatory cells and mediators, in particular eosinophils, which results in airway narrowing and associated bronchial hyper-responsiveness. […] Eosinophils play an important role in the pathophysiology of asthma, and their migration into the lungs is associated with inflammation and bronchoconstriction.
  • #41 A Review on Mechanism of Histamine Mediated Allergic Reactions: Therapeutic Role, Safety, and Clinical Efficacy of Cetirizine in Modern Allergy and Other Diseases Management – Biomedical and Pharmacology Journal
    https://biomedpharmajournal.org/vol18no1/a-review-on-mechanism-of-histamine-mediated-allergic-reactions-therapeutic-role-safety-and-clinical-efficacy-of-cetirizine-in-modern-allergy-and-other-diseases-management/
    Histamine-mediated allergic reactions are central to the pathogenesis of various allergic disorders, involving complex molecular mechanisms. […] This process triggers immediate hypersensitivity reactions, which manifest as common allergic symptoms. Inducing allergic inflammation largely depends on effector Th2 cells, which release cytokines like IL-4, IL-5, and IL-13, which promote eosinophilia, mucus secretion, and recruitment of inflammatory cells, thereby exacerbating allergic responses. […] Histamine release is a crucial phase in allergic responses, occurring when intracellular histamine stored in mast cell granules is released into the extracellular environment. This is initiated by antigen-antibody interactions, where FcRI-bound IgE on mast cells stimulates tyrosine-protein kinase activation.
  • #42 New Study Uncovers Mechanism Responsible For Seasonal Allergies | Consultant360
    https://www.consultant360.com/exclusives/new-study-uncovers-mechanism-responsible-seasonal-allergies
    Researchers have discovered an important mechanism in the process of becoming allergic to pollen that is responsible for the development of allergic asthma and seasonal allergies, according to a new study. […] Individuals who suffer from seasonal allergies and allergic asthma experience heightened responses to these allergens over the course of repeated exposures. […] They observed that when exposed to the allergen, the mice’s immune systems released proteins called chemokines with the purpose of attracting neutrophils to the site of the reaction. […] „These data suggest that when the body is forced to react to the presence of pollen in the airways, it recruits neutrophils that induce a state of continuous oxidative stress in the airways. This type of cellular stress from any cause can worsen allergic asthma,” researchers wrote. […] „We suggest that inhibiting recruitment of neutrophils by blocking chemokines may be a unique strategy for preventing pollen-induced allergic disorders,” they concluded.
  • #43 Effector mechanisms in allergic reactions – Immunobiology – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK27112/
    The ligation of cell-bound IgE antibody by specific antigen triggers activation of these cells at the site of antigen entry into the tissues. The release of inflammatory lipid mediators, cytokines, and chemokines at sites of IgE-triggered reactions results in the recruitment of eosinophils and basophils to augment the type I response. […] Mast cells express FcRI constitutively on their surface and are activated when antigens cross-link IgE bound to these receptors. Degranulation occurs within seconds, releasing a variety of preformed inflammatory mediators. […] On activation, mast cells synthesize and release chemokines, lipid mediators such as leukotrienes and platelet-activating factor (PAF), and additional cytokines such as IL-4 and IL-13 which perpetuate the TH2 response. These mediators contribute to both the acute and the chronic inflammatory responses.
  • #44 Allergic Reactions
    https://www.aaaai.org/tools-for-the-public/conditions-library/allergies/allergic-reactions
    Allergic reactions are actually a result of a chain reaction that begins in your genes and is expressed by your immune system. […] Your immune system identifies pollen as an invader or allergen. Your immune system overreacts by producing antibodies called Immunoglobulin E (IgE). These antibodies travel to cells that release chemicals, causing an allergic reaction. […] It is not yet fully understood why some substances trigger allergies and others do not, nor why some people have allergic reactions while others do not. […] A family history of allergies is the single most important factor that puts you at risk of developing allergic disease. […] Allergy symptoms are the result of a chain reaction that starts in your immune system. […] If you have a family history of allergies, you are at a much higher risk of developing allergic disease.
  • #45 Azthena logo with the word Azthena
    https://www.news-medical.net/health/Allergies-and-Genetics.aspx
    Specific gene variations that alter the encoding of epithelial cell-derived cytokines such as interleukin-33 and thymic stromal lymphopoietin may be involved in the pathogenesis of allergies. […] Additionally, variations in the ORMDL3 and GSDML genes have been linked to an increased risk of early-onset asthma. […] It is likely that each of these factors may play in the pathogenesis of allergies, particularly for individuals who have a genetic susceptibility to the condition.
  • #46 Azthena logo with the word Azthena
    https://www.news-medical.net/health/Allergies-and-Genetics.aspx
    Specific gene variations that alter the encoding of epithelial cell-derived cytokines such as interleukin-33 and thymic stromal lymphopoietin may be involved in the pathogenesis of allergies. […] Additionally, variations in the ORMDL3 and GSDML genes have been linked to an increased risk of early-onset asthma. […] It is likely that each of these factors may play in the pathogenesis of allergies, particularly for individuals who have a genetic susceptibility to the condition.
  • #47 Combattre les allergies – L’actu de l’Institut Pasteur
    https://www.pasteur.fr/en/home/research-journal/reports/tackling-allergies
    Apart from the specific case of anaphylactic shock, standard first-line allergy treatments are designed to address the symptoms. […] The idea is to teach the body to tolerate the allergen by giving the patient small doses of it (natural pollen extracts, mites, bee venom, etc.), via injection or sublingual delivery, over a period of several weeks or months and sometimes throughout their lifetime. […] We have shown how some bacteria in the microbiota specifically block the immune responses involved in allergic reactions. […] Several theories have been proposed to explain this trend. The „hygiene hypothesis” suggests that progress in hygiene is to blame despite having improved life expectancy by dramatically reducing the number of deaths from infectious diseases.
  • #48 Assessing the Mechanism of Immunotherapy for Allergy and Allergic Asthma: Effect of Viral Respiratory Infections on Pathogenesis and Clinical Course of Asthma and Allergy | FDA
    https://www.fda.gov/vaccines-blood-biologics/science-research-biologics/assessing-mechanism-immunotherapy-allergy-and-allergic-asthma-effect-viral-respiratory-infections
    Properly balanced, viral infection is locally contained. Improperly balanced, prolonged expression of IFNs or more likely, high expression of pro-inflammatory cytokines mediates autoinflammatory tissue destruction and promotes allergic sensitization or asthma. […] In genetically susceptible individuals, HDM are among the first environmental allergens to elicit allergic disease, and may initiate the allergic march towards multiple allergies and allergic asthma. […] We focus on factors that determine successful local immunity to respiratory viruses, and that shift the response from one that is primarily anti-viral towards a one that is pro-inflammatory.
  • #49 Unraveling the Mechanism of Ocular Allergies
    https://www.reviewofophthalmology.com/article/unraveling-the-mechanism-of-ocular-allergies
    „Our studies show that some environmental factors, such as certain microbial components that are produced by bacteria or fungi or viruses, would stimulate the corneal epithelial cells to produce levels of this cytokine called TSLP,” says Dr. Pflugfelder, an author of the study. „We found out that TSLP regulates the immune response toward an allergy type of response, which is called T-helper 2 or TH2 response. Therefore, it shows that for a long time, there has been a link between environmental factors and induction of allergy.” […] „There are receptors on cells called toll-like receptors, and there are 10 of those in human cells that have been identified,” says Dr. Pflugfelder. „They bind to these different microbial components and this stimulates a stress signaling response by the cell. So that is where we found that these microbial factors stimulated production of TSLP through the toll-like receptors,” he explains.
  • #50 Allergic Diseases: A Comprehensive Review on Risk Factors, Immunological Mechanisms, Link with COVID-19, Potential Treatments, and Role of Allergen Bioinformatics
    https://www.mdpi.com/1660-4601/18/22/12105
    They regulate the activation and recruitment of pro-inflammatory cells (mast cells and eosinophils) in mucosal target organs, as well as the class switching of IgE in B cells. […] Allergy symptoms and inflammation are triggered by these activations. […] The microbiota (intestinal microflora) are a collection of microorganisms, primarily bacteria, that form a complex ecosystem in the human digestive tract. […] The gut microbiota plays a significant role in the formation of immune system organs and help to identify host immune response patterns. […] Dysbiosis is described as a disruption in gut homeostasis caused by a change in the function and composition of the microbiota. […] Numerous studies suggest that dysbiosis intestinal, or quantitative and qualitative abnormalities in the microflora composition, may be a factor in the pathogenesis of a variety of disorders, including allergic disorders.
  • #51 Allergic Diseases: A Comprehensive Review on Risk Factors, Immunological Mechanisms, Link with COVID-19, Potential Treatments, and Role of Allergen Bioinformatics
    https://www.mdpi.com/1660-4601/18/22/12105
    They regulate the activation and recruitment of pro-inflammatory cells (mast cells and eosinophils) in mucosal target organs, as well as the class switching of IgE in B cells. […] Allergy symptoms and inflammation are triggered by these activations. […] The microbiota (intestinal microflora) are a collection of microorganisms, primarily bacteria, that form a complex ecosystem in the human digestive tract. […] The gut microbiota plays a significant role in the formation of immune system organs and help to identify host immune response patterns. […] Dysbiosis is described as a disruption in gut homeostasis caused by a change in the function and composition of the microbiota. […] Numerous studies suggest that dysbiosis intestinal, or quantitative and qualitative abnormalities in the microflora composition, may be a factor in the pathogenesis of a variety of disorders, including allergic disorders.
  • #52 Allergic Diseases: A Comprehensive Review on Risk Factors, Immunological Mechanisms, Link with COVID-19, Potential Treatments, and Role of Allergen Bioinformatics
    https://www.mdpi.com/1660-4601/18/22/12105
    There is mounting evidence that dysbiosis precedes the onset of allergic symptoms. […] The role of bacterial and viral infections in the development of allergic diseases is discussed later. […] Viral infections can have a variety of opposing effects on allergy and asthma development; depending on the circumstances, viruses can either protect against or trigger allergic disorders. […] The type of virus, age, intensity, timing, and location of the infection, as well as interactions with pollutants or allergens, have all been linked to allergic diseases development, particularly asthma, regarding viral infections. […] Although the mechanisms underlying the association of asthma and viral respiratory tract infection are not completely understood, recent reports indicate that epithelial cell viral infection could produce cytokines, such as IL-33 and IL-25, that interact with allergic inflammation, inducing both antigen-specific and innate T2 cell–related pathways.
  • #53 Combattre les allergies – L’actu de l’Institut Pasteur
    https://www.pasteur.fr/en/home/research-journal/reports/tackling-allergies
    Apart from the specific case of anaphylactic shock, standard first-line allergy treatments are designed to address the symptoms. […] The idea is to teach the body to tolerate the allergen by giving the patient small doses of it (natural pollen extracts, mites, bee venom, etc.), via injection or sublingual delivery, over a period of several weeks or months and sometimes throughout their lifetime. […] We have shown how some bacteria in the microbiota specifically block the immune responses involved in allergic reactions. […] Several theories have been proposed to explain this trend. The „hygiene hypothesis” suggests that progress in hygiene is to blame despite having improved life expectancy by dramatically reducing the number of deaths from infectious diseases.
  • #54 Allergic Diseases: A Comprehensive Review on Risk Factors, Immunological Mechanisms, Link with COVID-19, Potential Treatments, and Role of Allergen Bioinformatics
    https://www.mdpi.com/1660-4601/18/22/12105
    There is mounting evidence that dysbiosis precedes the onset of allergic symptoms. […] The role of bacterial and viral infections in the development of allergic diseases is discussed later. […] Viral infections can have a variety of opposing effects on allergy and asthma development; depending on the circumstances, viruses can either protect against or trigger allergic disorders. […] The type of virus, age, intensity, timing, and location of the infection, as well as interactions with pollutants or allergens, have all been linked to allergic diseases development, particularly asthma, regarding viral infections. […] Although the mechanisms underlying the association of asthma and viral respiratory tract infection are not completely understood, recent reports indicate that epithelial cell viral infection could produce cytokines, such as IL-33 and IL-25, that interact with allergic inflammation, inducing both antigen-specific and innate T2 cell–related pathways.
  • #55 Allergic Diseases: A Comprehensive Review on Risk Factors, Immunological Mechanisms, Link with COVID-19, Potential Treatments, and Role of Allergen Bioinformatics
    https://www.mdpi.com/1660-4601/18/22/12105
    The COVID-19 epidemic has been a burden for allergy professionals. […] The stress of the COVID-19 pandemic, therefore, may increase the psychiatric reaction in those who have preexisting allergic conditions. […] Bacteria play a dual role in allergies. […] They mainly concern protection, although certain species of bacteria stimulate allergic inflammation. […] Bacterial exposure has long been linked to allergy prevention. […] In recent decades, the hygiene theory has been bolstered by the discovery of a considerable decline in infectious diseases associated with a sharp increase in the frequency of allergy. […] Bacteria have been found to exhibit a variety of pro-allergenic activities (non-antigen-specific and antigen-specific). […] Hence, bacteria exert control over general allergy-inducing pathways and may become targets for type 2 immune responses defined by IgE antibodies and specific T2 cells.
  • #56 Allergic Diseases: A Comprehensive Review on Risk Factors, Immunological Mechanisms, Link with COVID-19, Potential Treatments, and Role of Allergen Bioinformatics
    https://www.mdpi.com/1660-4601/18/22/12105
    The COVID-19 epidemic has been a burden for allergy professionals. […] The stress of the COVID-19 pandemic, therefore, may increase the psychiatric reaction in those who have preexisting allergic conditions. […] Bacteria play a dual role in allergies. […] They mainly concern protection, although certain species of bacteria stimulate allergic inflammation. […] Bacterial exposure has long been linked to allergy prevention. […] In recent decades, the hygiene theory has been bolstered by the discovery of a considerable decline in infectious diseases associated with a sharp increase in the frequency of allergy. […] Bacteria have been found to exhibit a variety of pro-allergenic activities (non-antigen-specific and antigen-specific). […] Hence, bacteria exert control over general allergy-inducing pathways and may become targets for type 2 immune responses defined by IgE antibodies and specific T2 cells.
  • #57 Pathogenesis of allergic diseases and implications for therapeutic interventions | Signal Transduction and Targeted Therapy
    https://www.nature.com/articles/s41392-023-01344-4
    Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. […] The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. […] The pathogenesis of AD is mainly reflected by a complex interplay between epidermal barrier dysfunction, abnormal skin microbiota and dysregulated type 2 T cell immunity. […] FA is an IgE-dependent type I hypersensitivity to a specific food allergen.
  • #58 Pathogenesis of allergic diseases and implications for therapeutic interventions
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10039055/
    The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively.
  • #59 Pathogenesis of allergic diseases and implications for therapeutic interventions | Signal Transduction and Targeted Therapy
    https://www.nature.com/articles/s41392-023-01344-4
    The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function. […] The immunopathological profiles of AR and AAS are very similar in terms of eosinophil, mast cell and Th2 cell infiltration. […] In the AAS disease, mucosal pathological alterations comprise epithelial hyperplasia, goblet cell metaplasia and increased mucus generation. […] Allergens cross-link IgE that interact with mast cells, which further induces the release of multiple mediators (including histamine and leukotrienes), promotes arteriole dilation and vascular permeability, and causes pruritus, runny nose, mucus secretion, and pulmonary smooth muscle contraction. […] The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function.
  • #60 Pathogenesis of allergic diseases and implications for therapeutic interventions | Signal Transduction and Targeted Therapy
    https://www.nature.com/articles/s41392-023-01344-4
    The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function. […] The immunopathological profiles of AR and AAS are very similar in terms of eosinophil, mast cell and Th2 cell infiltration. […] In the AAS disease, mucosal pathological alterations comprise epithelial hyperplasia, goblet cell metaplasia and increased mucus generation. […] Allergens cross-link IgE that interact with mast cells, which further induces the release of multiple mediators (including histamine and leukotrienes), promotes arteriole dilation and vascular permeability, and causes pruritus, runny nose, mucus secretion, and pulmonary smooth muscle contraction. […] The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function.
  • #61 Allergic rhinitis – Wikipedia
    https://en.wikipedia.org/wiki/Allergic_rhinitis
    Allergic rhinitis, of which the seasonal type is called hay fever, is a type of inflammation in the nose that occurs when the immune system overreacts to allergens in the air. It is classified as a type I hypersensitivity reaction. […] The underlying mechanism involves IgE antibodies that attach to an allergen, and subsequently result in the release of inflammatory chemicals such as histamine from mast cells. […] The pathophysiology of allergic rhinitis involves Th2 Helper T cell and IgE mediated inflammation with overactive function of the adaptive and innate immune systems. The process begins when an aeroallergen penetrates the nasal mucosal barrier. […] The allergen is then engulfed by an antigen presenting cell (APC) (such as a dendritic cell). The APC then presents the antigen to a Naive CD4+ helper T cell stimulating it to differentiate into a Th2 helper T cell. The Th2 helper T cell then secretes inflammatory cytokines including IL-4, IL-5, IL-13, IL-14, and IL-31.
  • #62 Allergic rhinitis – Wikipedia
    https://en.wikipedia.org/wiki/Allergic_rhinitis
    Allergic rhinitis, of which the seasonal type is called hay fever, is a type of inflammation in the nose that occurs when the immune system overreacts to allergens in the air. It is classified as a type I hypersensitivity reaction. […] The underlying mechanism involves IgE antibodies that attach to an allergen, and subsequently result in the release of inflammatory chemicals such as histamine from mast cells. […] The pathophysiology of allergic rhinitis involves Th2 Helper T cell and IgE mediated inflammation with overactive function of the adaptive and innate immune systems. The process begins when an aeroallergen penetrates the nasal mucosal barrier. […] The allergen is then engulfed by an antigen presenting cell (APC) (such as a dendritic cell). The APC then presents the antigen to a Naive CD4+ helper T cell stimulating it to differentiate into a Th2 helper T cell. The Th2 helper T cell then secretes inflammatory cytokines including IL-4, IL-5, IL-13, IL-14, and IL-31.
  • #63 Pathogenesis of allergic diseases and implications for therapeutic interventions | Signal Transduction and Targeted Therapy
    https://www.nature.com/articles/s41392-023-01344-4
    Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. […] The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. […] The pathogenesis of AD is mainly reflected by a complex interplay between epidermal barrier dysfunction, abnormal skin microbiota and dysregulated type 2 T cell immunity. […] FA is an IgE-dependent type I hypersensitivity to a specific food allergen.
  • #64 Allergic Contact Dermatitis: Symptoms, Causes, and Treatment – DermNet
    https://dermnetnz.org/topics/allergic-contact-dermatitis
    Allergic contact dermatitis is a form of dermatitis/eczema caused by an allergic reaction to a material, called an allergen, in contact with the skin. The mechanism involves CD4+ T-lymphocytes, which recognise an antigen on the skin surface, releasing cytokines that activate the immune system and cause the dermatitis. […] Patients with atopic dermatitis associated with defective filaggrin (a structural protein in the stratum corneum) have a high risk of also developing allergic contact dermatitis. […] Allergic contact dermatitis starts as a localised reaction to an allergen in contact with the skin, but severe reactions may generalise due to autoeczematisation and can lead to erythroderma. […] Sometimes contact allergy arises only after the skin has been exposed to ultraviolet light. The rash is confined to sun-exposed areas even though the allergen may have been in contact with covered areas. This is called photocontact dermatitis. […] Contact allergy often persists lifelong so it is essential to identify the allergen and avoid touching it. Dermatitis may recur on re-exposure to the allergen.
  • #65 A Review on Mechanism of Histamine Mediated Allergic Reactions: Therapeutic Role, Safety, and Clinical Efficacy of Cetirizine in Modern Allergy and Other Diseases Management – Biomedical and Pharmacology Journal
    https://biomedpharmajournal.org/vol18no1/a-review-on-mechanism-of-histamine-mediated-allergic-reactions-therapeutic-role-safety-and-clinical-efficacy-of-cetirizine-in-modern-allergy-and-other-diseases-management/
    This review aims to provide a thorough analysis of the mechanisms underlying histamine-mediated allergic reactions, the molecular and pharmacological actions of cetirizine, and its clinical efficacy and safety profile, particularly in emerging allergic conditions. […] Cetirizine is used in the treatment of various types of allergic conditions. […] The rise in food allergies, particularly in children, has prompted investigations into the role of cetirizine as a potential therapy. […] Cetirizine has proven effective in reducing pruritus in AD patients by inhibiting histamine-mediated itching and reducing inflammatory markers like IL-4 and IL-13. […] Cetirizine has been found effective in treating both seasonal and perennial allergic conjunctivitis. […] Cetirizine has been reported as an effective treatment for managing mild-to-moderate drug-induced allergic reactions, especially in hospital settings, where its rapid onset of action can be beneficial in acute management.
  • #66 Pathogenesis of allergic diseases and implications for therapeutic interventions | Signal Transduction and Targeted Therapy
    https://www.nature.com/articles/s41392-023-01344-4
    Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. […] The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. […] The pathogenesis of AD is mainly reflected by a complex interplay between epidermal barrier dysfunction, abnormal skin microbiota and dysregulated type 2 T cell immunity. […] FA is an IgE-dependent type I hypersensitivity to a specific food allergen.
  • #67 Pathogenesis of allergic diseases and implications for therapeutic interventions
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10039055/
    Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. The pathogenesis of AD is mainly reflected by a complex interplay between epidermal barrier dysfunction, abnormal skin microbiota and dysregulated type 2 T cell immunity. FA is an IgE-dependent type I hypersensitivity to a specific food allergen. Its pathological process is divided into two stages: in the allergic sensitization stage, the initial exposure to the allergen results in tolerance breakdown, with subsequent generation of specific IgE, vasoactive substances and allergic response mediators such as histamine and platelet activating factor. The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function.
  • #68 Food allergy: immune mechanisms, diagnosis and immunotherapy | Nature Reviews Immunology
    https://www.nature.com/articles/nri.2016.111
    There are many forms of food allergy, the most common of which are IgE mediated. Common IgE-mediated food allergies include those to peanuts, tree nuts, cow’s milk, egg, soy, wheat, shellfish and fish. […] The immune system normally develops tolerance to food proteins, at least in part due to the actions of CD4+ regulatory T cells. […] Food allergy develops when the immune system mounts a T helper 2 (TH2) cell-mediated response against food epitopes. TH2 cell sensitization may occur initially at the skin, rather than in the gastrointestinal tract. […] Patients with established food allergy may become desensitized to food allergens by oral immunotherapy, which is thought to involve a shift from allergen-specific TH2 cells to CD4+ regulatory T cells, anergic cells and apoptotic cells. Typically, patients must continue regular consumption of food allergen to maintain desensitization.
  • #69 Food allergy: immune mechanisms, diagnosis and immunotherapy | Nature Reviews Immunology
    https://www.nature.com/articles/nri.2016.111
    There are many forms of food allergy, the most common of which are IgE mediated. Common IgE-mediated food allergies include those to peanuts, tree nuts, cow’s milk, egg, soy, wheat, shellfish and fish. […] The immune system normally develops tolerance to food proteins, at least in part due to the actions of CD4+ regulatory T cells. […] Food allergy develops when the immune system mounts a T helper 2 (TH2) cell-mediated response against food epitopes. TH2 cell sensitization may occur initially at the skin, rather than in the gastrointestinal tract. […] Patients with established food allergy may become desensitized to food allergens by oral immunotherapy, which is thought to involve a shift from allergen-specific TH2 cells to CD4+ regulatory T cells, anergic cells and apoptotic cells. Typically, patients must continue regular consumption of food allergen to maintain desensitization.
  • #70 Food allergy: immune mechanisms, diagnosis and immunotherapy | Nature Reviews Immunology
    https://www.nature.com/articles/nri.2016.111
    There are many forms of food allergy, the most common of which are IgE mediated. Common IgE-mediated food allergies include those to peanuts, tree nuts, cow’s milk, egg, soy, wheat, shellfish and fish. […] The immune system normally develops tolerance to food proteins, at least in part due to the actions of CD4+ regulatory T cells. […] Food allergy develops when the immune system mounts a T helper 2 (TH2) cell-mediated response against food epitopes. TH2 cell sensitization may occur initially at the skin, rather than in the gastrointestinal tract. […] Patients with established food allergy may become desensitized to food allergens by oral immunotherapy, which is thought to involve a shift from allergen-specific TH2 cells to CD4+ regulatory T cells, anergic cells and apoptotic cells. Typically, patients must continue regular consumption of food allergen to maintain desensitization.
  • #71 Antihistamine Types & Side Effects
    https://my.clevelandclinic.org/health/treatments/antihistamines
    Antihistamines are a class of medication that commonly treat allergy symptoms, like runny nose, sneezing and itchy eyes. […] Antihistamines work by blocking histamine receptors. […] Histamine is a chemical your immune system releases to send messages between different cells. Histamine has several functions, but its mainly known for its role in causing allergic and anaphylactic symptoms. […] By blocking the effects of histamine, antihistamines help prevent or manage these symptoms. […] Antihistamines can also help with certain digestive conditions and things like motion sickness and nausea. […] Antihistamines help millions of people with allergies manage their symptoms. […] Antihistamines are generally effective, though it may take time to find the one that works best for you.
  • #72 Antihistamine Types & Side Effects
    https://my.clevelandclinic.org/health/treatments/antihistamines
    Antihistamines are a class of medication that commonly treat allergy symptoms, like runny nose, sneezing and itchy eyes. […] Antihistamines work by blocking histamine receptors. […] Histamine is a chemical your immune system releases to send messages between different cells. Histamine has several functions, but its mainly known for its role in causing allergic and anaphylactic symptoms. […] By blocking the effects of histamine, antihistamines help prevent or manage these symptoms. […] Antihistamines can also help with certain digestive conditions and things like motion sickness and nausea. […] Antihistamines help millions of people with allergies manage their symptoms. […] Antihistamines are generally effective, though it may take time to find the one that works best for you.
  • #73 Antihistamine Types & Side Effects
    https://my.clevelandclinic.org/health/treatments/antihistamines
    Antihistamines are a class of medication that commonly treat allergy symptoms, like runny nose, sneezing and itchy eyes. […] Antihistamines work by blocking histamine receptors. […] Histamine is a chemical your immune system releases to send messages between different cells. Histamine has several functions, but its mainly known for its role in causing allergic and anaphylactic symptoms. […] By blocking the effects of histamine, antihistamines help prevent or manage these symptoms. […] Antihistamines can also help with certain digestive conditions and things like motion sickness and nausea. […] Antihistamines help millions of people with allergies manage their symptoms. […] Antihistamines are generally effective, though it may take time to find the one that works best for you.
  • #74 A Review on Mechanism of Histamine Mediated Allergic Reactions: Therapeutic Role, Safety, and Clinical Efficacy of Cetirizine in Modern Allergy and Other Diseases Management – Biomedical and Pharmacology Journal
    https://biomedpharmajournal.org/vol18no1/a-review-on-mechanism-of-histamine-mediated-allergic-reactions-therapeutic-role-safety-and-clinical-efficacy-of-cetirizine-in-modern-allergy-and-other-diseases-management/
    Cetirizine, a second-generation antihistamine, has a well-established safety profile, particularly for its long-term use. […] Cetirizine maintains its efficacy over time. […] The lack of significant sedative effects allows patients to maintain their normal activities and productivity, thus enhancing adherence to treatment and overall satisfaction. […] Future research should prioritize personalized treatment approaches for cetirizine, particularly considering how individual genetic variations impact drug metabolism and allergic responses. […] As allergies continue to rise globally, cetirizine’s role as a key antihistamine will remain vital, with ongoing research needed to optimize its clinical utility in diverse allergic diseases.
  • #75 A Review on Mechanism of Histamine Mediated Allergic Reactions: Therapeutic Role, Safety, and Clinical Efficacy of Cetirizine in Modern Allergy and Other Diseases Management – Biomedical and Pharmacology Journal
    https://biomedpharmajournal.org/vol18no1/a-review-on-mechanism-of-histamine-mediated-allergic-reactions-therapeutic-role-safety-and-clinical-efficacy-of-cetirizine-in-modern-allergy-and-other-diseases-management/
    Cetirizine, a second-generation antihistamine, has a well-established safety profile, particularly for its long-term use. […] Cetirizine maintains its efficacy over time. […] The lack of significant sedative effects allows patients to maintain their normal activities and productivity, thus enhancing adherence to treatment and overall satisfaction. […] Future research should prioritize personalized treatment approaches for cetirizine, particularly considering how individual genetic variations impact drug metabolism and allergic responses. […] As allergies continue to rise globally, cetirizine’s role as a key antihistamine will remain vital, with ongoing research needed to optimize its clinical utility in diverse allergic diseases.
  • #76 Hypersensitivity | PPT
    https://www.slideshare.net/slideshow/hypersensitivity-24449005/24449005
    Hypersensitivity refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity These reactions may be damaging, uncomfortable, or occasionally fatal. TYPE I IMMEDIATE, ATOPIC, ANAPHYLACTIC TYPE II ANTIBODY DEPENDANT TYPE III IMMUNE COMPLEX TYPE IV CELL MEDIATED / DELAYED TYPE OF HYPERSENSITIVITY Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity. The reaction may involve skin (urticaria and eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) and gastrointestinal tract (gastroenteritis). The reaction may cause a range of symptoms from minor inconvenience to death. The reaction usually takes 15 – 30 minutes from the time of exposure to the antigen, although sometimes it may have a delayed onset (10 – 12 hours). Mediated by IgE antibody to specific antigens The primary cellular component in this hypersensitivity is the mast cell or basophil. The reaction is amplified and/or modified by platelets, neutrophils and eosinophils. Mast cells stimulated and release histamine. ALLERGEN: Allergens are nonparasite antigens that can stimulate a type I hypersensitivity response. Atopy is the term for the genetic trait to have a predisposition for localized anaphylaxis. Atopic individuals have higher levels of IgE and eosinophils. Initial introduction of antigen produces an antibody response. More specifically, the type of antigen and the way in which it is administered induce the synthesis of IgE antibody in particular. Immunoglobulin IgE binds very specifically to receptors on the surface of mast cells, which remain circulating. Reintroduced antigen interacts with IgE on mast cells causing the cells to degranulate and release large amounts of histamine, lipid mediators and chemotactic factors that cause smooth muscle contraction, vasodilation, increased vascular permeability, broncoconstriction and edema. These reactions occur very suddenly, causing death. Histamine Cytokines TNF- , IL-1, IL-6. Chemoattractants for Neutrophils and Eosinophils. Enzymes tryptase, chymase, cathepsin. Changes in connective tissue matrix, tissue breakdown Leukotrienes Prostaglandins. Diagnostic tests for immediate hypersensitivity include skin (prick and intradermal) tests, measurement of total IgE and specific IgE antibodies against the suspected allergens. Total IgE and specific IgE antibodies are measured by a modification of enzyme immunoassay (ELISA). Increased IgE levels are indicative of an atopic condition, although IgE may be elevated in some non-atopic diseases (e.g., myelomas, helminthic infection, etc.). Drugs. Non-steroidal anti-inflammatories Antihistamines block histamine receptors. Steroids Theophylline OR epinephrine -prolongs or increases cAMP levels in mast cells which inhibits degranulation. Immunotherapy Desensitization (hyposensitization) also known as allergy shots. Repeated injections of allergen to reduce the IgE on Mast cells and produce IgG. Type II hypersensitivity is also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues. The antigens are normally endogenous, although exogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity. Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia are such examples. Penicillin allergy also belong to this class. The reaction time is minutes to hours. Type II hypersensitivity is primarily mediated by antibodies of the IgM or IgG classes and complement. Phagocytes may also play a role. The lesion contains antibody, complement and neutrophils. Rh factor incompatibility IgG abs to Rh an innocuous rbc antigen Rh+ baby born to Rh- mother first time fine. 2nd time can have abs to Rh from 1st pregnancy. Ab crosses placenta and baby kills its own rbcs. Treat mother with ab to Rh antigen right after birth and mother never makes its own immune response. Diagnostic tests include detection of circulating antibody against the tissues involved and the presence of antibody and complement in the lesion (biopsy) by immunofluorescence. The staining pattern is normally smooth and linear, such as that seen in Goodpasture’s nephritis (renal and lung basement membrane) Treatment involves anti-inflammatory and immunosuppressive agents. Antigen antibody immune complexes. IgG mediated Large amount of antigen and antibodies form complexes in blood. If not eliminated can deposit in capillaries or joints and trigger inflammation. The reaction may be general (e.g., serum sickness) or may involve individual organs including skin (e.g., systemic lupus erythematosus, Arthus reaction), kidneys (e.g., lupus nephritis), lungs (e.g., aspergillosis), joints (e.g., rheumatoid arthritis) or other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganisms. The reaction may take 3 – 10 hours after exposure to the antigen. It is mediated by soluble immune complexes. They are mostly of the IgG class, although IgM may also be involved. The antigen may be exogenous (chronic bacterial, viral or parasitic infections), or endogenous (non-organ specific autoimmunity: e.g., systemic lupus erythematosus, SLE). The antigen is soluble and not attached to the organ involved. PMNs and macrophages bind to immune complexes via FcR and phagocytize the complexes. BUT If unable to phagocytize the immune complexes can cause inflammation via C activation — C3a C4a, C5a and „frustrated phagocytes”. Diagnosis involves examination of tissue biopsies for deposits of immunoglobulin and complement by immunofluorescence microscopy. The presence of immune complexes in serum and depletion in the level of complement are also diagnostic. Treatment includes anti-inflammatory agents. Reaction involves sensitized T cells and release of its lymphokines as mediators and amplifiers Mediated by cells rather than antibodies Clinical states: Contact dermatitis, Transplant rejection, Granuloma. Th1 cells release cytokines to activate macrophages causing inflammation and tissue damage. Continued macrophage activation can cause chronic inflammation resulting in tissue lesions, scarring, and granuloma formation. Response starts after 48 -72 hrs. Delayed hypersensitivity reactions Type Reaction time Clinical appearance Histology Antigen and site Contact dermatitis 48-72 hr eczema lymphocytes, followed by macrophages; edema of epidermis epidermal (organic chemicals, poison ivy, heavy metals, etc.) tuberculin 48-72 hr local induration lymphocytes, monocytes, macrophages intradermal (tuberculin, lepromin, etc.) granuloma 21-28 days hardening macrophages, epitheloid and giant cells, fibrosis persistent antigen or foreign body presence (tuberculosis, leprosy, etc.) Diagnostic tests in vivo include delayed cutaneous reaction (e.g. Montoux test and patch test (for contact dermatitis). In vitro tests for delayed hypersensitivity include mitogenic response, lympho-cytotoxicity and IL-2 production. Corticosteroids and other immunosuppressive agents are used in treatment. Comparison of Different Types of hypersensitivity characteristics type-I anaphylactic type-II (cytotoxic) type-III (immune complex) type-IV (delayed type) antibody IgE IgG, IgM IgG, IgM None antigen exogenous cell surface soluble tissues organs response time 15-30 minutes minutes-hours 3-8 hours 48-72 hours appearance weal flare lysis and necrosis erythema and edema, necrosis erythema and induration histology basophils and eosinophil antibody and complement complement and neutrophils monocytes and lymphocytes transferred with antibody antibody antibody T-cells examples allergic asthma, hay fever erythroblastosis fetalis, Goodpasture’s nephritis SLE, farmer’s lung disease tuberculin test, poison ivy, granuloma.
  • #77 Allergic Rhinitis (AR) Causes & Mechanisms | Haleon HealthPartner
    https://www.haleonhealthpartner.com/en-us/respiratory-health/conditions/allergic-rhinitis-conditions-home/allergic-rhinitis/allergic-rhinitis-causes-mechanism/
    The bodys immune response to allergens includes a series of early- and late-phase reactionsthe allergic cascade. There are several allergic mediators involved in this cascade, not just histamines. […] The end result is the allergic response consisting of a range of symptoms such as rhinorrhea (runny nose), sneezing, congestion, and pruritus (itching)2 […] INSs, often used as first-line treatment for patients with mild persistent or moderate-to-severe symptoms, work locally in the nasal mucosa to block multiple mediators involved in the allergic cascade, including histamine, cytokines, leukotrienes, chemokines, prostaglandins, and tryptase.
  • #78 Montelukast (Singulair): Uses, Side Effects, Interactions, Pictures, Warnings & Dosing – WebMD
    https://www.webmd.com/drugs/2/drug-6478-8277/montelukast-oral/montelukast-oral/details
    Montelukast is also used to help control the symptoms of allergies such as sneezing, stuffy, runny, and itchy nose. […] Montelukast helps improve asthma symptoms by blocking substances in the body called leukotrienes that cause inflammation and swelling. […] Severe Allergic Reactions. Montelukast may cause allergic reactions, which can be serious. […] Eosinophilia and Systemic Vasculitis. Montelukast can increase certain white blood cells called eosinophils and cause swelling of the blood vessels throughout the body, a condition called systemic vasculitis. […] Allergies to Ingredients. People who are allergic to any of the following should not take montelukast.
  • #79 Montelukast (Singulair): Uses, Side Effects, Interactions, Pictures, Warnings & Dosing – WebMD
    https://www.webmd.com/drugs/2/drug-6478-8277/montelukast-oral/montelukast-oral/details
    Montelukast is also used to help control the symptoms of allergies such as sneezing, stuffy, runny, and itchy nose. […] Montelukast helps improve asthma symptoms by blocking substances in the body called leukotrienes that cause inflammation and swelling. […] Severe Allergic Reactions. Montelukast may cause allergic reactions, which can be serious. […] Eosinophilia and Systemic Vasculitis. Montelukast can increase certain white blood cells called eosinophils and cause swelling of the blood vessels throughout the body, a condition called systemic vasculitis. […] Allergies to Ingredients. People who are allergic to any of the following should not take montelukast.
  • #80 Mast Cell Activation Syndrome (MCAS)
    https://www.aaaai.org/conditions-treatments/related-conditions/mcas
    Mast cell mediators increase during the episode. Those mediators should be measured during acute episodes and at baseline looking for elevations during symptoms. […] The immediate goal is to provide relief for the patient. Lack of response to these treatments suggests that MCAS is not present. […] Omalizumab (which blocks binding of IgE to its receptors) has been reported to reduce mast cell reactivity and sensitivity to activation which can reduce anaphylactic episodes. […] These criteria require the presence of anaphylactic symptoms, the elevation of mast cell mediators during symptoms and the resolution of symptoms with appropriate treatment(s).
  • #81 FAQs | FASENRA® (benralizumab) Subcutaneous Injection
    https://www.fasenra.com/faq
    FASENRA helps prevent asthma attacks (exacerbations) and may improve your breathing. Medicines such as FASENRA reduce blood eosinophils.* Eosinophils are a type of white blood cell that may contribute to your asthma. […] The mechanism of action of FASENRA in asthma is not fully understood. […] FASENRA is designed to target and remove eosinophils, a key cause of asthma. The mechanism of action of FASENRA in asthma is not fully understood.
  • #82 FAQs | FASENRA® (benralizumab) Subcutaneous Injection
    https://www.fasenra.com/faq
    FASENRA helps prevent asthma attacks (exacerbations) and may improve your breathing. Medicines such as FASENRA reduce blood eosinophils.* Eosinophils are a type of white blood cell that may contribute to your asthma. […] The mechanism of action of FASENRA in asthma is not fully understood. […] FASENRA is designed to target and remove eosinophils, a key cause of asthma. The mechanism of action of FASENRA in asthma is not fully understood.
  • #83 Allergy | British Society for Immunology
    https://www.immunology.org/policy-and-public-affairs/briefings-and-position-statements/allergy
    In the case of allergy, binding of an allergen to IgE-mast cells results in their rapid degranulation and the release of inflammatory compounds, including histamine, which contribute to local inflammation and the symptoms associated with allergy. […] Allergy is widespread in the UK and worldwide and the number of people affected and experiencing severe allergic symptoms continues to increase, particularly in the developed world. […] The idea that exposure to infectious agents may decrease the risk of allergy was first introduced in 1989. […] One of these is the skewing towards an immune profile of T helper 2 cells (Th2 cells) over T helper 1 cells. […] Allergy immunotherapy (AIT), or desensitisation involves administration of a particular allergen, given in gradually increasing doses, eventually developing immunity or tolerance to the allergen.
  • #84 Allergy | British Society for Immunology
    https://www.immunology.org/policy-and-public-affairs/briefings-and-position-statements/allergy
    During AIT, the immune system’s responses change. These changes may include producing less IgE, producing ‘blocking’ IgG antibodies, and producing more regulatory T cells, promoting tolerance and a less active immune response. […] However, the exact mechanism behind desensitisation is not yet known and it is likely that different patients exhibit different immune profiles following the treatment.
  • #85 Researchers identify mechanism underlying allergic itching, and show it can be blocked | ScienceDaily
    https://www.sciencedaily.com/releases/2024/09/240904131044.htm
    Our data suggest that this pathway is also present in humans, which raises the possibility that by targeting the IL-3-mediated signaling pathway, we can generate novel therapeutics for preventing an allergy. […] If we can determine the specific factors that activate GD3 cells and create this IL-3-mediated circuit, we might be able to intervene in those factors and not only understand allergic sensitization but prevent it.
  • #86 Unraveling the Mechanism of Ocular Allergies
    https://www.reviewofophthalmology.com/article/unraveling-the-mechanism-of-ocular-allergies
    „Allergy research in general is increasingly focusing on the union of the innate and adaptive immune systems in the pathogenesis of the disease,” Dr. Barney says. „The ocular surface has been shown to have pathogen-recognition receptors, a key element in recognition of microbial products that we are all exposed to. We are witnessing research into the effect that microbial product recognition has in the ocular surface undergoing an allergic reaction. Additionally, regulatory T-cell contribution to the initiation of and continuation of control over the allergic inflammation of the ocular surface is a valuable area of investigation.” […] Researchers are continuing to uncover the mechanisms behind allergic eye disease, an abnormal immune hypersensitivity response to allergens. Allergic eye disease is characterized by IgE-mediated and/or T-lymphocyte-mediated immune hypersensitivity reactions that lead to an immune response, resulting in the clinical manifestation of ocular allergy.
  • #87 Unraveling the Mechanism of Ocular Allergies
    https://www.reviewofophthalmology.com/article/unraveling-the-mechanism-of-ocular-allergies
    „Allergy research in general is increasingly focusing on the union of the innate and adaptive immune systems in the pathogenesis of the disease,” Dr. Barney says. „The ocular surface has been shown to have pathogen-recognition receptors, a key element in recognition of microbial products that we are all exposed to. We are witnessing research into the effect that microbial product recognition has in the ocular surface undergoing an allergic reaction. Additionally, regulatory T-cell contribution to the initiation of and continuation of control over the allergic inflammation of the ocular surface is a valuable area of investigation.” […] Researchers are continuing to uncover the mechanisms behind allergic eye disease, an abnormal immune hypersensitivity response to allergens. Allergic eye disease is characterized by IgE-mediated and/or T-lymphocyte-mediated immune hypersensitivity reactions that lead to an immune response, resulting in the clinical manifestation of ocular allergy.
  • #88 Researchers Identify Mechanism Underlying Allergic Itching, and Show It Can Be Blocked | Mass General Brigham
    https://www.massgeneralbrigham.org/en/about/newsroom/press-releases/researchers-identify-mechanism-underlying-allergic-itching
    The researchers found that a poorly understood specific immune cell type in the skin, that they called GD3 cells, produce a molecule called IL-3 in response to environmental triggers that include the microbes that normally live on the skin. […] IL-3 acts directly on a subset of itch-inducing sensory neurons to prime their responsiveness to even low levels of protease allergens from common sources like house dust mites, environmental molds and mosquitos. […] The researchers found that this process involves a signaling pathway that boosts the production of certain molecules, leading to the start of an allergic reaction. […] Since the type of immune cells in the mouse model is similar to that of humans, the authors conclude these findings may explain the pathways role in human allergies.
  • #89 Researchers Identify Mechanism Underlying Allergic Itching, and Show It Can Be Blocked | Mass General Brigham
    https://www.massgeneralbrigham.org/en/about/newsroom/press-releases/researchers-identify-mechanism-underlying-allergic-itching
    The researchers found that a poorly understood specific immune cell type in the skin, that they called GD3 cells, produce a molecule called IL-3 in response to environmental triggers that include the microbes that normally live on the skin. […] IL-3 acts directly on a subset of itch-inducing sensory neurons to prime their responsiveness to even low levels of protease allergens from common sources like house dust mites, environmental molds and mosquitos. […] The researchers found that this process involves a signaling pathway that boosts the production of certain molecules, leading to the start of an allergic reaction. […] Since the type of immune cells in the mouse model is similar to that of humans, the authors conclude these findings may explain the pathways role in human allergies.
  • #90 Mechanism found for destruction of key allergy-inducing complexes, researchers say | News Center
    https://med.stanford.edu/news/all-news/2012/10/mechanism-found-for-destruction-of-key-allergy-inducing-complexes-researchers-say
    Researchers have learned how a man-made molecule destroys complexes that induce allergic responses, which could lead to interventions for a host of acute allergic reactions. […] The new inhibitor disarms IgE antibodies, pivotal players in acute allergies, by detaching the antibody from its partner in crime, a molecule called FcR. […] The key to actively disabling the allergic response lies in the separation of IgE from the FcRs on the surface of mast cells. […] The collaboration of the two groups resulted in the characterization of DARPin E2-79, an inhibitor that goes beyond mere blockade to actively disassemble the IgE-FcR power couple. […] The researchers found that E2-79 hastens the separation of the two molecules by taking advantage of a moment of weakness in the relationship between IgE and FcR. […] E2-79 is the first molecule to display these IgE stripping characteristics. […] The discovery of E2-79’s mechanism of IgE inhibition could lead to rapid discoveries from other labs as well.
  • #91 Mechanism found for destruction of key allergy-inducing complexes, researchers say | News Center
    https://med.stanford.edu/news/all-news/2012/10/mechanism-found-for-destruction-of-key-allergy-inducing-complexes-researchers-say
    Researchers have learned how a man-made molecule destroys complexes that induce allergic responses, which could lead to interventions for a host of acute allergic reactions. […] The new inhibitor disarms IgE antibodies, pivotal players in acute allergies, by detaching the antibody from its partner in crime, a molecule called FcR. […] The key to actively disabling the allergic response lies in the separation of IgE from the FcRs on the surface of mast cells. […] The collaboration of the two groups resulted in the characterization of DARPin E2-79, an inhibitor that goes beyond mere blockade to actively disassemble the IgE-FcR power couple. […] The researchers found that E2-79 hastens the separation of the two molecules by taking advantage of a moment of weakness in the relationship between IgE and FcR. […] E2-79 is the first molecule to display these IgE stripping characteristics. […] The discovery of E2-79’s mechanism of IgE inhibition could lead to rapid discoveries from other labs as well.
  • #92 The Rockefeller University » New clues to the mechanism behind food tolerance and allergies
    https://www.rockefeller.edu/news/37240-new-clues-to-the-mechanism-behind-food-tolerance-and-allergies/
    Now, new research identifies specific gut cell types that communicate with T cells prompting them to tolerate, attack, or simply ignore and explains how these opposing responses are triggered. […] The findings, published in Science, give scientists a new understanding of how the intestinal immune system keeps the gut in balance, and may ultimately shed light on the root causes and mechanisms of food allergies and intestinal diseases. […] The intestinal immune system is complicated machinery. Tolerance to food begins with antigen presenting cells, or APCs, instructing T cells to stand down. […] After optimizing LIPSTIC for the task, Canesso and colleagues succeeded in pinpointing those APCs that promote tolerance a process primarily handled by two types: cDC1s and Rort+ APCs. […] They also uncovered how infections of the intestines can cause interference, demonstrating in mice that the parasitic worm Strongyloides venezuelensis shifts the balance away from tolerance promoting APCs and toward those that promote inflammation.
  • #93 The Rockefeller University » New clues to the mechanism behind food tolerance and allergies
    https://www.rockefeller.edu/news/37240-new-clues-to-the-mechanism-behind-food-tolerance-and-allergies/
    Now, new research identifies specific gut cell types that communicate with T cells prompting them to tolerate, attack, or simply ignore and explains how these opposing responses are triggered. […] The findings, published in Science, give scientists a new understanding of how the intestinal immune system keeps the gut in balance, and may ultimately shed light on the root causes and mechanisms of food allergies and intestinal diseases. […] The intestinal immune system is complicated machinery. Tolerance to food begins with antigen presenting cells, or APCs, instructing T cells to stand down. […] After optimizing LIPSTIC for the task, Canesso and colleagues succeeded in pinpointing those APCs that promote tolerance a process primarily handled by two types: cDC1s and Rort+ APCs. […] They also uncovered how infections of the intestines can cause interference, demonstrating in mice that the parasitic worm Strongyloides venezuelensis shifts the balance away from tolerance promoting APCs and toward those that promote inflammation.
  • #94 Pathogenesis of allergic diseases and implications for therapeutic interventions | Signal Transduction and Targeted Therapy
    https://www.nature.com/articles/s41392-023-01344-4
    The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function. […] The immunopathological profiles of AR and AAS are very similar in terms of eosinophil, mast cell and Th2 cell infiltration. […] In the AAS disease, mucosal pathological alterations comprise epithelial hyperplasia, goblet cell metaplasia and increased mucus generation. […] Allergens cross-link IgE that interact with mast cells, which further induces the release of multiple mediators (including histamine and leukotrienes), promotes arteriole dilation and vascular permeability, and causes pruritus, runny nose, mucus secretion, and pulmonary smooth muscle contraction. […] The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function.
  • #95 Pathogenesis of allergic diseases and implications for therapeutic interventions
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10039055/
    Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. The pathogenesis of AD is mainly reflected by a complex interplay between epidermal barrier dysfunction, abnormal skin microbiota and dysregulated type 2 T cell immunity. FA is an IgE-dependent type I hypersensitivity to a specific food allergen. Its pathological process is divided into two stages: in the allergic sensitization stage, the initial exposure to the allergen results in tolerance breakdown, with subsequent generation of specific IgE, vasoactive substances and allergic response mediators such as histamine and platelet activating factor. The pathogenesis of allergic diseases is complex, involving many factors such as genetics, epigenetics, environmental factors, microecology and the body’s immune function.
  • #96 The pathophysiology of allergic responses | Nursing Times
    https://www.nursingtimes.net/respiratory/the-pathophysiology-of-allergic-responses-16-05-2006/
    Allergy is the clinical expression of atopy – the physical symptoms of allergy related to exposure. […] The immune response is dependent on the bodys two subsets of T-lymphocytes, known as T helper cells TH1 and TH2. […] In atopic individuals, TH2 cells and their mediators encourage the immune system to recognise allergens as an invader, and mount a response against them. […] For allergy to exist, allergen sensitisation must first occur. […] The antigen-presenting cells come into contact with the allergen which, in people predisposed to atopy, is perceived to be an invader. […] After the period of sensitisation described above there is a period of latency, and on subsequent re-exposure to the allergen the allergic response is triggered: allergen cross-links with the IgE on the surfaces of the mast cell or basophil, causing the cell to degranulate or release inflammatory mediators.
  • #97 The complex pathophysiology of allergic rhinitis: scientific rationale for the development of an alternative treatment option | Allergy, Asthma & Clinical Immunology | Full Text
    https://aacijournal.biomedcentral.com/articles/10.1186/s13223-018-0314-1
    Allergic rhinitis (AR) poses a global health problem and can be challenging to treat. […] The pathophysiology of AR is complex, comprising an early- and late-phase allergic response. […] The early-phase reaction is characterised by mast cell degranulation. […] The late-phase reaction develops over a period of hours after exposure to an allergen. It is characterised by cellular recruitment of basophils, neutrophils, T-lymphocytes, monocytes, and eosinophils, and by the release of multiple mediators, including cytokines, prostaglandins, and leukotrienes, which perpetuate the inflammatory response. […] The pharmacological profiles of available treatments for AR show that there are a number of pathophysiological gaps within the AR pharmacopeia. […] Pathophysiological gaps associated with the various AR treatment options mean that many patients remain symptomatic despite treatment. […] MP-AzeFlu blocks two important pathophysiological pathways involved in the early- and late-phase reactions in the disease, providing rapid relief from all symptoms associated with AR.
  • #98 Pathogenesis of allergic diseases and implications for therapeutic interventions | Signal Transduction and Targeted Therapy
    https://www.nature.com/articles/s41392-023-01344-4
    Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. […] The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. […] The pathogenesis of AD is mainly reflected by a complex interplay between epidermal barrier dysfunction, abnormal skin microbiota and dysregulated type 2 T cell immunity. […] FA is an IgE-dependent type I hypersensitivity to a specific food allergen.
  • #99 The pathophysiology of allergic responses | Nursing Times
    https://www.nursingtimes.net/respiratory/the-pathophysiology-of-allergic-responses-16-05-2006/
    The early-phase reaction After sensitisation to an allergen has occurred, and on subsequent re-exposure, cross-linking of allergen on IgE displayed on the surfaces of mast cells in the nasal mucosa causes degranulation. […] The late-phase reaction After the early response in the nose following allergen exposure, inflammatory cells continue to be recruited. […] As with the asthmatic late response, eosinophils play an important role in the late-phase response in the nose, with the enzymes and proteins released causing tissue damage and further inflammation. […] An understanding of the pathophysiology of allergic disease is crucial in assisting in the management of allergic disease and symptoms.
  • #100 Insights into the Mechanisms underlying the Pathogenesis, Regulation, Prevention and Treatment of Allergic Disease | Frontiers Research Topic
    https://www.frontiersin.org/research-topics/7958/insights-into-the-mechanisms-underlying-the-pathogenesis-regulation-prevention-and-treatment-of-allergic-disease/magazine
    The balance between tolerance and inflammation involves a complex interplay between various cell types (both immune and non-immune), different molecular pathways, as well as various environmental and epigenetic factors. […] The goal of this Research Topic is to increase our understanding of the pathogenesis and treatment of allergic diseases in light of recent advances in the field, and with a specific emphasis on molecular and cellular mechanisms regulating immunity, genetics, and the environment.