Materiały źródłowe

• #1 Pathology and pathogenesis of sarcoidosis – UpToDate

  https://www.uptodate.com/contents/pathology-and-pathogenesis-of-sarcoidosis

  Sarcoidosis is a multisystem disorder of unknown etiology characterized by the accumulation of T lymphocytes, mononuclear phagocytes, and noncaseating granulomas in involved tissues. […] The pathology and pathogenesis of sarcoidosis will be reviewed here. […] Sarcoidosis is a multisystem disease that involves the lungs in 90 percent of cases. It has a predilection for the upper lobes of the lung and bronchovascular bundles more than other lung compartments, although it can affect any area. […] On histopathology, classic sarcoidosis granulomas are non-necrotizing with a tightly packed central area composed of macrophages, epithelioid cells, multinucleated giant cells, and T lymphocytes that are CD4 positive. […] The central areas are surrounded by CD8 and CD4 positive T lymphocytes, B lymphocytes, monocytes, mast cells, and fibroblasts, which in turn may be surrounded by lamellar rings of hyaline collagen.

• #2 Sarcoidosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK430687/

  Sarcoidosis is a multisystem disorder of unknown etiology characterized by noncaseating granulomas in organs. […] It is an inflammatory disease of unknown etiology that manifests as noncaseating granulomas in multiple systems. Various associations have been described, including occupational and environmental exposures to beryllium, dust, and other agents causing asthma. […] Pathogenesis of cutaneous sarcoidosis is poorly understood and attributable to both genetic and environmental factors. A key role in the development of sarcoidosis is played by T cells as they promote cellular immune reaction and are usually associated with an inverted CD4/CD8 ratio. […] Cytokines, including Th1, IL-2, IL6, IL 8, IL12, IL 18, IL 27, and interferon (IFN) gamma and tumor necrosis factor (TNF) alpha are closely associated with sarcoidosis. Few of these are implicated in granuloma formation with macrophage and epithelioid accumulation, activation, and aggregation.

• #3 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  Sarcoidosis is characterized by non-infectious non-caseating granulomas, comprised primarily of macrophages that differentiate to epithelioid cells, which subsequently fuse to form multinucleated giant cells. CD4+ T helper cells, the specificity of which is unknown, are interspersed in the granuloma while CD8+ T cells, regulatory T cells (Tregs), fibroblasts, and B cells surround the periphery. This heterogeneous cell population suggests that both innate and adaptive immune responses contribute to the onset and the progression of the disease. To date, however, the pathogenesis of sarcoidosis represents an unresolved immunological paradox. In sarcoidosis, affected organs present an intense immune response, yet at the same time, a state of immune anergy is established, as indicated by a reduced delayed-type hypersensitivity to tuberculin and common antigens.

• #4 Sarcoidosis – Wikipedia

  https://en.wikipedia.org/wiki/Sarcoidosis

  The exact cause of sarcoidosis is not known. The current working hypothesis is, in genetically susceptible individuals, sarcoidosis is caused through alteration to the immune response after exposure to an environmental, occupational, or infectious agent. […] Granulomatous inflammation is characterized primarily by the accumulation of macrophages and activated T-lymphocytes, with increased production of key inflammatory mediators, tumor necrosis factor alpha (TNF), interferon gamma, interleukin 2 (IL-2), IL-8, IL-10, IL-12, IL-18, IL-23 and transforming growth factor beta (TGF-), indicative of a T helper cell-mediated immune response. […] Sarcoidosis has paradoxical effects on inflammatory processes; it is characterized by increased macrophage and CD4 helper T-cell activation, resulting in accelerated inflammation, but immune response to antigen challenges such as tuberculin is suppressed. This paradoxic state of simultaneous hyper- and hypoactivity is suggestive of a state of anergy. The anergy may also be responsible for the increased risk of infections and cancer.

• #5 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://www.mdpi.com/2077-0383/9/8/2363

  Sarcoidosis is characterized by non-infectious non-caseating granulomas, comprised primarily of macrophages that differentiate to epithelioid cells, which subsequently fuse to form multinucleated giant cells. CD4+ T helper cells, the specificity of which is unknown, are interspersed in the granuloma while CD8+ T cells, regulatory T cells (Tregs), fibroblasts, and B cells surround the periphery. This heterogeneous cell population suggests that both innate and adaptive immune responses contribute to the onset and the progression of the disease. To date, however, the pathogenesis of sarcoidosis represents an unresolved immunological paradox. In sarcoidosis, affected organs present an intense immune response, yet at the same time, a state of immune anergy is established, as indicated by a reduced delayed-type hypersensitivity to tuberculin and common antigens.

• #6 Host-microbe interactions in the pathogenesis and clinical course of sarcoidosis | Journal of Biomedical Science | Full Text

  https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-019-0537-6

  Sarcoidosis is a rare inflammatory disease characterized by the development of granulomas in various organs, especially in the lungs and lymph nodes. […] Current evidence suggests that, in genetically predisposed individuals, an excessive immune response to unknown antigen/s is crucial for the development of sarcoidosis. […] In addition, accumulating evidence indicate that certain microorganisms, especially Cutibacterium acne (C. acne) and mycobacterium tuberculosis (mTB) may be implicated in the development of sarcoidosis, and thus various authors have proposed the possibility of including antibiotics as part of the standard treatment of this disease. […] Moreover, given the structural similarities of certain mycobacterial proteins, especially heat shock proteins of mycobacterium tuberculosis (mTB-hsp) with human heat shock proteins (HSPs), it has been proposed that the exposure to mycobacterial antigens, via either natural infection, or by vaccination with BCG, may trigger an autoimmune response leading to sarcoidosis, in genetically prone individuals.

• #7 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  Sarcoidosis is characterized by non-infectious non-caseating granulomas, comprised primarily of macrophages that differentiate to epithelioid cells, which subsequently fuse to form multinucleated giant cells. CD4+ T helper cells, the specificity of which is unknown, are interspersed in the granuloma while CD8+ T cells, regulatory T cells (Tregs), fibroblasts, and B cells surround the periphery. This heterogeneous cell population suggests that both innate and adaptive immune responses contribute to the onset and the progression of the disease. To date, however, the pathogenesis of sarcoidosis represents an unresolved immunological paradox. In sarcoidosis, affected organs present an intense immune response, yet at the same time, a state of immune anergy is established, as indicated by a reduced delayed-type hypersensitivity to tuberculin and common antigens.

• #8 Pathology and pathogenesis of sarcoidosis – UpToDate

  https://www.uptodate.com/contents/pathology-and-pathogenesis-of-sarcoidosis

  Sarcoidosis is a multisystem disorder of unknown etiology characterized by the accumulation of T lymphocytes, mononuclear phagocytes, and noncaseating granulomas in involved tissues. […] The pathology and pathogenesis of sarcoidosis will be reviewed here. […] Sarcoidosis is a multisystem disease that involves the lungs in 90 percent of cases. It has a predilection for the upper lobes of the lung and bronchovascular bundles more than other lung compartments, although it can affect any area. […] On histopathology, classic sarcoidosis granulomas are non-necrotizing with a tightly packed central area composed of macrophages, epithelioid cells, multinucleated giant cells, and T lymphocytes that are CD4 positive. […] The central areas are surrounded by CD8 and CD4 positive T lymphocytes, B lymphocytes, monocytes, mast cells, and fibroblasts, which in turn may be surrounded by lamellar rings of hyaline collagen.

• #9 Pathology and pathogenesis of sarcoidosis – UpToDate

  https://www.uptodate.com/contents/pathology-and-pathogenesis-of-sarcoidosis

  Sarcoidosis is a multisystem disorder of unknown etiology characterized by the accumulation of T lymphocytes, mononuclear phagocytes, and noncaseating granulomas in involved tissues. […] The pathology and pathogenesis of sarcoidosis will be reviewed here. […] Sarcoidosis is a multisystem disease that involves the lungs in 90 percent of cases. It has a predilection for the upper lobes of the lung and bronchovascular bundles more than other lung compartments, although it can affect any area. […] On histopathology, classic sarcoidosis granulomas are non-necrotizing with a tightly packed central area composed of macrophages, epithelioid cells, multinucleated giant cells, and T lymphocytes that are CD4 positive. […] The central areas are surrounded by CD8 and CD4 positive T lymphocytes, B lymphocytes, monocytes, mast cells, and fibroblasts, which in turn may be surrounded by lamellar rings of hyaline collagen.

• #10 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  Sarcoidosis is characterized by non-infectious non-caseating granulomas, comprised primarily of macrophages that differentiate to epithelioid cells, which subsequently fuse to form multinucleated giant cells. CD4+ T helper cells, the specificity of which is unknown, are interspersed in the granuloma while CD8+ T cells, regulatory T cells (Tregs), fibroblasts, and B cells surround the periphery. This heterogeneous cell population suggests that both innate and adaptive immune responses contribute to the onset and the progression of the disease. To date, however, the pathogenesis of sarcoidosis represents an unresolved immunological paradox. In sarcoidosis, affected organs present an intense immune response, yet at the same time, a state of immune anergy is established, as indicated by a reduced delayed-type hypersensitivity to tuberculin and common antigens.

• #11 Pathology and pathogenesis of sarcoidosis – UpToDate

  https://www.uptodate.com/contents/pathology-and-pathogenesis-of-sarcoidosis

  Additional histopathologic features of sarcoidosis granulomas that may be present include asteroid bodies, Schaumann bodies, and birefringent crystalline particles (calcium oxalate and other calcium salts). […] In rare patients with necrotizing sarcoid granulomatosis, the histopathology shows perivascular masses composed of confluent granulomas and necrosis of lung parenchyma.

• #12 Pathology and pathogenesis of sarcoidosis – UpToDate

  https://www.uptodate.com/contents/pathology-and-pathogenesis-of-sarcoidosis/print

  Additional histopathologic features of sarcoidosis granulomas that may be present include asteroid bodies, Schaumann bodies, and birefringent crystalline particles (calcium oxalate and other calcium salts). […] In rare patients with necrotizing sarcoid granulomatosis, the histopathology shows perivascular masses composed of confluent granulomas and necrosis of lung parenchyma.

• #13 Pathology and pathogenesis of sarcoidosis – UpToDate

  https://www.uptodate.com/contents/pathology-and-pathogenesis-of-sarcoidosis

  Additional histopathologic features of sarcoidosis granulomas that may be present include asteroid bodies, Schaumann bodies, and birefringent crystalline particles (calcium oxalate and other calcium salts). […] In rare patients with necrotizing sarcoid granulomatosis, the histopathology shows perivascular masses composed of confluent granulomas and necrosis of lung parenchyma.

• #14 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  Alveolar macrophages (AMs) are involved both in innate and adaptive immune responses in sarcoidosis. AMs produce a range of pro-inflammatory cytokines, such as tumor necrosis factor- (TNF-), which drives granuloma formation in sarcoidosis. In addition, AMs function as antigen-presenting cells (APCs), interacting with T-cells via human leukocyte antigen (HLA) molecules and T-cell receptors. Activation of the mammalian target of rapamycin complex 1 (mTORC1) pathway in macrophages promotes excessive granuloma formation in mice and is associated with macrophage proliferation and disease progression in patients with sarcoidosis. An analysis of peripheral blood monocytes from sarcoidosis patients found enrichment of activated monocytes available to populate sites of granulomatous inflammation and a higher prevalence of cells expressing CD11c, possibly representing a subpopulation of monocyte-derived cells that could differentiate to dendritic cells, thus linking innate and adaptive responses in sarcoidosis. There is an increased number of phagocytic monocytes in the blood of sarcoidosis patients to control subjects. Similarly, circulating monocytes also display higher Toll Like Receptor TLR2 and TLR4 expression, inducing Th1 and Th2 responses, respectively.

• #15 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  Alveolar macrophages (AMs) are involved both in innate and adaptive immune responses in sarcoidosis. AMs produce a range of pro-inflammatory cytokines, such as tumor necrosis factor- (TNF-), which drives granuloma formation in sarcoidosis. In addition, AMs function as antigen-presenting cells (APCs), interacting with T-cells via human leukocyte antigen (HLA) molecules and T-cell receptors. Activation of the mammalian target of rapamycin complex 1 (mTORC1) pathway in macrophages promotes excessive granuloma formation in mice and is associated with macrophage proliferation and disease progression in patients with sarcoidosis. An analysis of peripheral blood monocytes from sarcoidosis patients found enrichment of activated monocytes available to populate sites of granulomatous inflammation and a higher prevalence of cells expressing CD11c, possibly representing a subpopulation of monocyte-derived cells that could differentiate to dendritic cells, thus linking innate and adaptive responses in sarcoidosis. There is an increased number of phagocytic monocytes in the blood of sarcoidosis patients to control subjects. Similarly, circulating monocytes also display higher Toll Like Receptor TLR2 and TLR4 expression, inducing Th1 and Th2 responses, respectively.

• #16 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  Alveolar macrophages (AMs) are involved both in innate and adaptive immune responses in sarcoidosis. AMs produce a range of pro-inflammatory cytokines, such as tumor necrosis factor- (TNF-), which drives granuloma formation in sarcoidosis. In addition, AMs function as antigen-presenting cells (APCs), interacting with T-cells via human leukocyte antigen (HLA) molecules and T-cell receptors. Activation of the mammalian target of rapamycin complex 1 (mTORC1) pathway in macrophages promotes excessive granuloma formation in mice and is associated with macrophage proliferation and disease progression in patients with sarcoidosis. An analysis of peripheral blood monocytes from sarcoidosis patients found enrichment of activated monocytes available to populate sites of granulomatous inflammation and a higher prevalence of cells expressing CD11c, possibly representing a subpopulation of monocyte-derived cells that could differentiate to dendritic cells, thus linking innate and adaptive responses in sarcoidosis. There is an increased number of phagocytic monocytes in the blood of sarcoidosis patients to control subjects. Similarly, circulating monocytes also display higher Toll Like Receptor TLR2 and TLR4 expression, inducing Th1 and Th2 responses, respectively.

• #17

  https://www.jci.org/articles/view/175264

  Sarcoidosis is a complex immune-mediated disease characterized by clusters of immune cells called granulomas. […] In this Review, we perform a mechanistic interrogation of the immune activities that contribute to granuloma formation in sarcoidosis and compare these processes with its closest mimic, tuberculosis, highlighting shared and divergent immune activities. […] The immune profile in sarcoidosis is dominated by Th1 cell overactivity. […] We interrogate the immune activities contributing to granuloma formation in sarcoidosis and compare these to TB, its closest mimic clinically and histopathologically. […] In sarcoidosis, chronic upregulated mTORC1 signaling in macrophages is proposed as a major factor in persistence of granuloma. […] Linke et al. found that activation of mTORC1 in myeloid cells (via myeloid-specific deletion of Tsc2) initiated and maintained granuloma formation via increased macrophage proliferation and inhibition of apoptosis in vivo.

• #18 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  Alveolar macrophages (AMs) are involved both in innate and adaptive immune responses in sarcoidosis. AMs produce a range of pro-inflammatory cytokines, such as tumor necrosis factor- (TNF-), which drives granuloma formation in sarcoidosis. In addition, AMs function as antigen-presenting cells (APCs), interacting with T-cells via human leukocyte antigen (HLA) molecules and T-cell receptors. Activation of the mammalian target of rapamycin complex 1 (mTORC1) pathway in macrophages promotes excessive granuloma formation in mice and is associated with macrophage proliferation and disease progression in patients with sarcoidosis. An analysis of peripheral blood monocytes from sarcoidosis patients found enrichment of activated monocytes available to populate sites of granulomatous inflammation and a higher prevalence of cells expressing CD11c, possibly representing a subpopulation of monocyte-derived cells that could differentiate to dendritic cells, thus linking innate and adaptive responses in sarcoidosis. There is an increased number of phagocytic monocytes in the blood of sarcoidosis patients to control subjects. Similarly, circulating monocytes also display higher Toll Like Receptor TLR2 and TLR4 expression, inducing Th1 and Th2 responses, respectively.

• #19 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  Alveolar macrophages (AMs) are involved both in innate and adaptive immune responses in sarcoidosis. AMs produce a range of pro-inflammatory cytokines, such as tumor necrosis factor- (TNF-), which drives granuloma formation in sarcoidosis. In addition, AMs function as antigen-presenting cells (APCs), interacting with T-cells via human leukocyte antigen (HLA) molecules and T-cell receptors. Activation of the mammalian target of rapamycin complex 1 (mTORC1) pathway in macrophages promotes excessive granuloma formation in mice and is associated with macrophage proliferation and disease progression in patients with sarcoidosis. An analysis of peripheral blood monocytes from sarcoidosis patients found enrichment of activated monocytes available to populate sites of granulomatous inflammation and a higher prevalence of cells expressing CD11c, possibly representing a subpopulation of monocyte-derived cells that could differentiate to dendritic cells, thus linking innate and adaptive responses in sarcoidosis. There is an increased number of phagocytic monocytes in the blood of sarcoidosis patients to control subjects. Similarly, circulating monocytes also display higher Toll Like Receptor TLR2 and TLR4 expression, inducing Th1 and Th2 responses, respectively.

• #20 Systemic Manifestations of Sarcoidosis | SpringerLink

  https://link.springer.com/10.1007/978-3-319-90495-5_302-1

  Sarcoidosis is a systemic granulomatous inflammatory disease of unknown etiology with a heterogeneous clinical presentation, which seems to result from an interplay between environmental factors in genetically predisposed individuals. […] The main hallmark of sarcoidosis is the development of noncaseating granulomas in the lungs, lymph nodes, and skin typically; however, unpredictable affection of any organ system is possible, which makes diagnosis often difficult for health providers. […] Current concepts of the pathogenesis of sarcoidosis. […] New concepts in the pathogenesis of sarcoidosis (accepted manuscript). […] Molecular evidence for the role of mycobacteria in sarcoidosis: a meta-analysis. […] Disordered Toll-like receptor 2 responses in the pathogenesis of pulmonary sarcoidosis.

• #21 Evidence for local dendritic cell activation in pulmonary sarcoidosis | Respiratory Research | Full Text

  https://respiratory-research.biomedcentral.com/articles/10.1186/1465-9921-13-33

  Sarcoidosis is a granulomatous disease characterized by a seemingly exaggerated immune response against a difficult to discern antigen. Dendritic cells (DCs) are pivotal antigen presenting cells thought to play an important role in the pathogenesis. […] We hypothesized that at the site of disease DCs are mature, immunocompetent and involved in granuloma formation. […] Taken together, these findings indicate that mDCs from the BAL from sarcoidosis patients were functional and did not display diminished immunoreactivity, when compared with mDCs from healthy controls. […] Taken together these results indicate that pulmonary sarcoidosis is associated with increased numbers of mature, functionally competent DCs that intrinsically induce increased levels of a central mediator in sarcoidosis, TNF.

• #22 Evidence for local dendritic cell activation in pulmonary sarcoidosis | Respiratory Research | Full Text

  https://respiratory-research.biomedcentral.com/articles/10.1186/1465-9921-13-33

  Sarcoidosis is a granulomatous disease characterized by a seemingly exaggerated immune response against a difficult to discern antigen. Dendritic cells (DCs) are pivotal antigen presenting cells thought to play an important role in the pathogenesis. […] We hypothesized that at the site of disease DCs are mature, immunocompetent and involved in granuloma formation. […] Taken together, these findings indicate that mDCs from the BAL from sarcoidosis patients were functional and did not display diminished immunoreactivity, when compared with mDCs from healthy controls. […] Taken together these results indicate that pulmonary sarcoidosis is associated with increased numbers of mature, functionally competent DCs that intrinsically induce increased levels of a central mediator in sarcoidosis, TNF.

• #23 Evidence for local dendritic cell activation in pulmonary sarcoidosis | Respiratory Research | Full Text

  https://respiratory-research.biomedcentral.com/articles/10.1186/1465-9921-13-33

  Granuloma formation was associated with an increase in number and maturation status of DCs, providing evidence for the involvement of DCs in granuloma formation or maintenance in sarcoidosis. […] Our results strongly support the notion that mDCs are involved in granuloma formation and maintenance in sarcoidosis, rather than the alternative that DCs are defective in supporting the adaptive immune system in antigen clearance. […] Intrinsic genetic alterations in key APCs may underlie the exaggerated immune response to a hard to discern antigen that is characteristic of sarcoidosis.

• #24 Evidence for local dendritic cell activation in pulmonary sarcoidosis | Respiratory Research | Full Text

  https://respiratory-research.biomedcentral.com/articles/10.1186/1465-9921-13-33

  Granuloma formation was associated with an increase in number and maturation status of DCs, providing evidence for the involvement of DCs in granuloma formation or maintenance in sarcoidosis. […] Our results strongly support the notion that mDCs are involved in granuloma formation and maintenance in sarcoidosis, rather than the alternative that DCs are defective in supporting the adaptive immune system in antigen clearance. […] Intrinsic genetic alterations in key APCs may underlie the exaggerated immune response to a hard to discern antigen that is characteristic of sarcoidosis.

• #25 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  T-cells, particularly activated CD4+ T-cells, play a key role in the inflammation in sarcoidosis. Different subsets of CD4+ helper T cells participate in the immunopathogenesis of sarcoidosis. The main feature of the acute disease is represented by a Th1/Th17/regulatory T cells (Tregs)-driven inflammatory process involving macrophages both as antigen-presenting cells and key effectors. As discussed above, when triggered by factors as yet unidentified, APCs such as DCs release cytokines (e.g., IL-12) and other inflammatory factors, leading to a milieu that induces recruitment and activation of Th1 CD4+ T-cells and monocytes to the lungs. In sarcoidosis, the lung homes up to ten times as many CD4+ T-cells as the peripheral blood, thus leading to an elevated CD4/CD8 ratio as measured in BAL fluid. The CD4+ T cells that trigger the granuloma formation are strongly Th1 polarized. Upon TCR activation, the expression of IFN in CD4+ T cells becomes more pronounced. In response to IL-12, CD4+ T-cell production of IL-4 and IL-13 (cytokines that facilitate the fibroproliferative response) is inhibited. IL-12 and IL-18 act synergistically to promote the formation of sarcoid granulomas.

• #26 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  T-cells, particularly activated CD4+ T-cells, play a key role in the inflammation in sarcoidosis. Different subsets of CD4+ helper T cells participate in the immunopathogenesis of sarcoidosis. The main feature of the acute disease is represented by a Th1/Th17/regulatory T cells (Tregs)-driven inflammatory process involving macrophages both as antigen-presenting cells and key effectors. As discussed above, when triggered by factors as yet unidentified, APCs such as DCs release cytokines (e.g., IL-12) and other inflammatory factors, leading to a milieu that induces recruitment and activation of Th1 CD4+ T-cells and monocytes to the lungs. In sarcoidosis, the lung homes up to ten times as many CD4+ T-cells as the peripheral blood, thus leading to an elevated CD4/CD8 ratio as measured in BAL fluid. The CD4+ T cells that trigger the granuloma formation are strongly Th1 polarized. Upon TCR activation, the expression of IFN in CD4+ T cells becomes more pronounced. In response to IL-12, CD4+ T-cell production of IL-4 and IL-13 (cytokines that facilitate the fibroproliferative response) is inhibited. IL-12 and IL-18 act synergistically to promote the formation of sarcoid granulomas.

• #27 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  T-cells, particularly activated CD4+ T-cells, play a key role in the inflammation in sarcoidosis. Different subsets of CD4+ helper T cells participate in the immunopathogenesis of sarcoidosis. The main feature of the acute disease is represented by a Th1/Th17/regulatory T cells (Tregs)-driven inflammatory process involving macrophages both as antigen-presenting cells and key effectors. As discussed above, when triggered by factors as yet unidentified, APCs such as DCs release cytokines (e.g., IL-12) and other inflammatory factors, leading to a milieu that induces recruitment and activation of Th1 CD4+ T-cells and monocytes to the lungs. In sarcoidosis, the lung homes up to ten times as many CD4+ T-cells as the peripheral blood, thus leading to an elevated CD4/CD8 ratio as measured in BAL fluid. The CD4+ T cells that trigger the granuloma formation are strongly Th1 polarized. Upon TCR activation, the expression of IFN in CD4+ T cells becomes more pronounced. In response to IL-12, CD4+ T-cell production of IL-4 and IL-13 (cytokines that facilitate the fibroproliferative response) is inhibited. IL-12 and IL-18 act synergistically to promote the formation of sarcoid granulomas.

• #28 Sarcoidosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/301914-overview

  T cells play a central role in the development of sarcoidosis, as they likely propagate an excessive cellular immune reaction. For example, there is an accumulation of CD4 cells accompanied by the release of interleukin (IL)2 at sites of disease activity. This may manifest clinically by an inverted CD4/CD8 ratio. Pulmonary sarcoidosis is frequently characterized by a CD4+/CD8+ ratio of at least 3.5 in bronchoalveolar lavage fluid (BALF), although up to 40% of the cases present a normal or even decreased ratio, thus limiting its diagnostic value. Increased production of TH1 cytokines, such as interferon, is also a feature. […] Moreover, both tumor necrosis factor (TNF) and TNF receptors are increased in this disease. The importance of TNF in propagating inflammation in sarcoidosis has been demonstrated by the efficacy of anti-TNF agents, such as pentoxifylline and infliximab, in treating this disease.

• #29 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  T-cells, particularly activated CD4+ T-cells, play a key role in the inflammation in sarcoidosis. Different subsets of CD4+ helper T cells participate in the immunopathogenesis of sarcoidosis. The main feature of the acute disease is represented by a Th1/Th17/regulatory T cells (Tregs)-driven inflammatory process involving macrophages both as antigen-presenting cells and key effectors. As discussed above, when triggered by factors as yet unidentified, APCs such as DCs release cytokines (e.g., IL-12) and other inflammatory factors, leading to a milieu that induces recruitment and activation of Th1 CD4+ T-cells and monocytes to the lungs. In sarcoidosis, the lung homes up to ten times as many CD4+ T-cells as the peripheral blood, thus leading to an elevated CD4/CD8 ratio as measured in BAL fluid. The CD4+ T cells that trigger the granuloma formation are strongly Th1 polarized. Upon TCR activation, the expression of IFN in CD4+ T cells becomes more pronounced. In response to IL-12, CD4+ T-cell production of IL-4 and IL-13 (cytokines that facilitate the fibroproliferative response) is inhibited. IL-12 and IL-18 act synergistically to promote the formation of sarcoid granulomas.

• #30 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  T-cells, particularly activated CD4+ T-cells, play a key role in the inflammation in sarcoidosis. Different subsets of CD4+ helper T cells participate in the immunopathogenesis of sarcoidosis. The main feature of the acute disease is represented by a Th1/Th17/regulatory T cells (Tregs)-driven inflammatory process involving macrophages both as antigen-presenting cells and key effectors. As discussed above, when triggered by factors as yet unidentified, APCs such as DCs release cytokines (e.g., IL-12) and other inflammatory factors, leading to a milieu that induces recruitment and activation of Th1 CD4+ T-cells and monocytes to the lungs. In sarcoidosis, the lung homes up to ten times as many CD4+ T-cells as the peripheral blood, thus leading to an elevated CD4/CD8 ratio as measured in BAL fluid. The CD4+ T cells that trigger the granuloma formation are strongly Th1 polarized. Upon TCR activation, the expression of IFN in CD4+ T cells becomes more pronounced. In response to IL-12, CD4+ T-cell production of IL-4 and IL-13 (cytokines that facilitate the fibroproliferative response) is inhibited. IL-12 and IL-18 act synergistically to promote the formation of sarcoid granulomas.

• #31 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7465477/

  T-cells, particularly activated CD4+ T-cells, play a key role in the inflammation in sarcoidosis. Different subsets of CD4+ helper T cells participate in the immunopathogenesis of sarcoidosis. The main feature of the acute disease is represented by a Th1/Th17/regulatory T cells (Tregs)-driven inflammatory process involving macrophages both as antigen-presenting cells and key effectors. As discussed above, when triggered by factors as yet unidentified, APCs such as DCs release cytokines (e.g., IL-12) and other inflammatory factors, leading to a milieu that induces recruitment and activation of Th1 CD4+ T-cells and monocytes to the lungs. In sarcoidosis, the lung homes up to ten times as many CD4+ T-cells as the peripheral blood, thus leading to an elevated CD4/CD8 ratio as measured in BAL fluid. The CD4+ T cells that trigger the granuloma formation are strongly Th1 polarized. Upon TCR activation, the expression of IFN in CD4+ T cells becomes more pronounced. In response to IL-12, CD4+ T-cell production of IL-4 and IL-13 (cytokines that facilitate the fibroproliferative response) is inhibited. IL-12 and IL-18 act synergistically to promote the formation of sarcoid granulomas.

• #32 Host-microbe interactions in the pathogenesis and clinical course of sarcoidosis | Journal of Biomedical Science | Full Text

  https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-019-0537-6

  The key pathogenic component of sarcoidosis is the development of noncaseating granulomas that can arise in different organs. Current evidence suggests that a combination of genetic predisposition and environmental conditions play a central role in the excessive immune reaction leading to the development of sarcoidosis. […] Granulomas constitute an excessive immune response aimed to control or eliminate an uncharacterized antigen. […] The immune signature of sarcoidosis is the excessive immune response mediated by CD4+ type 1 helper-like cells (Th1-cells), including hyperactivation of Th1-cells and increased levels of Th1 cytokines. […] Another subset of CD4T-lymphocytes, involvement in granuloma induction or maintenance in sarcoidosis are Th17 cells, as documented by the elevated numbers of IL-17, IL-22 and IFN- secreting CD4T-lymphocytes found in the blood of patients with sarcoidosis.

• #33 Sarcoidosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/301914-overview

  In addition to T cells, B cells also play a role. There is evidence of B cell hyperreactivity with immunoglobulin production. […] Soluble HLA class I antigens levels in serum and BALF are higher in patients with sarcoidosis. These levels tend to be significantly higher in active than in inactive stages and correlate with angiotensin-converting enzyme (ACE) levels. […] Active sarcoidosis has also been associated with plasmatic hypergammaglobulinemia. B-cell accumulation has been shown in pulmonary lesions, and a beneficial effect with anti-CD20 monoclonal antibody therapy has been reported in select patients. […] Glycoprotein KL-6 and surfactant protein D (SP-D) derived from alveolar type II cells and bronchiolar epithelial cells are significantly increased in pulmonary sarcoidosis and correlate with the percentage of lymphocytes in BALF, reflecting an inflammatory response in sarcoidosis. However, there is no significant correlation between KL-6 or SP-D levels and chest radiography findings, ACE levels, or CD4/CD8 ratio in BALF. KL-6 has been shown to be predictive of increased pulmonary parenchymal infiltration. […] A study by Facco et al suggests that Th17 cells may play a role in the pathogenesis and progression of sarcoidosis; these cells were noted to be present in the blood, BALF samples, and lung tissue from patients with sarcoidosis, particularly in those with the active form of the disease.

• #34 Host-microbe interactions in the pathogenesis and clinical course of sarcoidosis | Journal of Biomedical Science | Full Text

  https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-019-0537-6

  The key pathogenic component of sarcoidosis is the development of noncaseating granulomas that can arise in different organs. Current evidence suggests that a combination of genetic predisposition and environmental conditions play a central role in the excessive immune reaction leading to the development of sarcoidosis. […] Granulomas constitute an excessive immune response aimed to control or eliminate an uncharacterized antigen. […] The immune signature of sarcoidosis is the excessive immune response mediated by CD4+ type 1 helper-like cells (Th1-cells), including hyperactivation of Th1-cells and increased levels of Th1 cytokines. […] Another subset of CD4T-lymphocytes, involvement in granuloma induction or maintenance in sarcoidosis are Th17 cells, as documented by the elevated numbers of IL-17, IL-22 and IFN- secreting CD4T-lymphocytes found in the blood of patients with sarcoidosis.

• #35 Host-microbe interactions in the pathogenesis and clinical course of sarcoidosis | Journal of Biomedical Science | Full Text

  https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-019-0537-6

  Regulatory cells (Treg cells), which are defined as CD4+CD25brightFoxP3+ have been also implicated in the pathogenesis of sarcoidosis. […] The appearance of familiarly clustered cases of sarcoidosis and the racial differences in disease incidence and clinical progression support a possible link of genetics with the development of this disease. […] The most strongly and consistently associated risk factor for sarcoidosis is the major histocompatibility complex (MHC) region, comprising of HLA class I and class II genes, being HLA class II variants, particularly HLA-DRB1 and DQB1 the alleles most prevalently reported in association with sarcoidosis. […] Despite that numerous genetic risk factors in association with sarcoidosis have been identified, in the majority of cases, the biologic functions of specific variants and their precise interaction with environmental exposures remain unknown.

• #36 Sarcoidosis – Wikipedia

  https://en.wikipedia.org/wiki/Sarcoidosis

  The regulatory T-lymphocytes in the periphery of sarcoid granulomas appear to suppress IL-2 secretion, which is hypothesized to cause the state of anergy by preventing antigen-specific memory responses. […] While TNF is widely believed to play an important role in the formation of granulomas, sarcoidosis can and does still develop in those being treated with TNF antagonists like etanercept. […] B cells also likely play a role in the pathophysiology of sarcoidosis.

• #37 Introductory Chapter: Sarcoidosis – New Perspectives | IntechOpen

  https://www.intechopen.com/chapters/82125

  Several studies suggest that not only unknown antigens are responsible for sarcoidosis, but also genetic susceptibility, environmental factors, and in some instances, autoimmunity. […] In the most cases in sarcoidosis patients, the growth of these granulomas establishes the primary abnormality. […] It is presumed that in sarcoidosis, infiltrating T-reg cells fail to reduce the exaggerated inflammatory response, thereby contributing to persistence and integrity of granuloma. […] Also, T-reg cells release transforming growth factor- (TGF-), which may contribute to fibrosis and granuloma. […] Th17 cells are linked to the sarcoidosis pathogenesis and are recruited to the disease site and involved in the construction of the granuloma. […] The balance between Th17 and T-reg cells is thought to be disrupted in sarcoidosis and also, is an important factor in sarcoidosis prognosis.

• #38 Introductory Chapter: Sarcoidosis – New Perspectives | IntechOpen

  https://www.intechopen.com/chapters/82125

  Several studies suggest that not only unknown antigens are responsible for sarcoidosis, but also genetic susceptibility, environmental factors, and in some instances, autoimmunity. […] In the most cases in sarcoidosis patients, the growth of these granulomas establishes the primary abnormality. […] It is presumed that in sarcoidosis, infiltrating T-reg cells fail to reduce the exaggerated inflammatory response, thereby contributing to persistence and integrity of granuloma. […] Also, T-reg cells release transforming growth factor- (TGF-), which may contribute to fibrosis and granuloma. […] Th17 cells are linked to the sarcoidosis pathogenesis and are recruited to the disease site and involved in the construction of the granuloma. […] The balance between Th17 and T-reg cells is thought to be disrupted in sarcoidosis and also, is an important factor in sarcoidosis prognosis.

• #39 Introductory Chapter: Sarcoidosis – New Perspectives | IntechOpen

  https://www.intechopen.com/chapters/82125

  Several studies suggest that not only unknown antigens are responsible for sarcoidosis, but also genetic susceptibility, environmental factors, and in some instances, autoimmunity. […] In the most cases in sarcoidosis patients, the growth of these granulomas establishes the primary abnormality. […] It is presumed that in sarcoidosis, infiltrating T-reg cells fail to reduce the exaggerated inflammatory response, thereby contributing to persistence and integrity of granuloma. […] Also, T-reg cells release transforming growth factor- (TGF-), which may contribute to fibrosis and granuloma. […] Th17 cells are linked to the sarcoidosis pathogenesis and are recruited to the disease site and involved in the construction of the granuloma. […] The balance between Th17 and T-reg cells is thought to be disrupted in sarcoidosis and also, is an important factor in sarcoidosis prognosis.

• #40 Sarcoidosis – Wikipedia

  https://en.wikipedia.org/wiki/Sarcoidosis

  The exact cause of sarcoidosis is not known. The current working hypothesis is, in genetically susceptible individuals, sarcoidosis is caused through alteration to the immune response after exposure to an environmental, occupational, or infectious agent. […] Granulomatous inflammation is characterized primarily by the accumulation of macrophages and activated T-lymphocytes, with increased production of key inflammatory mediators, tumor necrosis factor alpha (TNF), interferon gamma, interleukin 2 (IL-2), IL-8, IL-10, IL-12, IL-18, IL-23 and transforming growth factor beta (TGF-), indicative of a T helper cell-mediated immune response. […] Sarcoidosis has paradoxical effects on inflammatory processes; it is characterized by increased macrophage and CD4 helper T-cell activation, resulting in accelerated inflammation, but immune response to antigen challenges such as tuberculin is suppressed. This paradoxic state of simultaneous hyper- and hypoactivity is suggestive of a state of anergy. The anergy may also be responsible for the increased risk of infections and cancer.

• #41 Sarcoidosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK430687/

  Sarcoidosis is a multisystem disorder of unknown etiology characterized by noncaseating granulomas in organs. […] It is an inflammatory disease of unknown etiology that manifests as noncaseating granulomas in multiple systems. Various associations have been described, including occupational and environmental exposures to beryllium, dust, and other agents causing asthma. […] Pathogenesis of cutaneous sarcoidosis is poorly understood and attributable to both genetic and environmental factors. A key role in the development of sarcoidosis is played by T cells as they promote cellular immune reaction and are usually associated with an inverted CD4/CD8 ratio. […] Cytokines, including Th1, IL-2, IL6, IL 8, IL12, IL 18, IL 27, and interferon (IFN) gamma and tumor necrosis factor (TNF) alpha are closely associated with sarcoidosis. Few of these are implicated in granuloma formation with macrophage and epithelioid accumulation, activation, and aggregation.

• #42 Sarcoidosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK430687/

  Sarcoidosis is a multisystem disorder of unknown etiology characterized by noncaseating granulomas in organs. […] It is an inflammatory disease of unknown etiology that manifests as noncaseating granulomas in multiple systems. Various associations have been described, including occupational and environmental exposures to beryllium, dust, and other agents causing asthma. […] Pathogenesis of cutaneous sarcoidosis is poorly understood and attributable to both genetic and environmental factors. A key role in the development of sarcoidosis is played by T cells as they promote cellular immune reaction and are usually associated with an inverted CD4/CD8 ratio. […] Cytokines, including Th1, IL-2, IL6, IL 8, IL12, IL 18, IL 27, and interferon (IFN) gamma and tumor necrosis factor (TNF) alpha are closely associated with sarcoidosis. Few of these are implicated in granuloma formation with macrophage and epithelioid accumulation, activation, and aggregation.

• #43 Sarcoidosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK430687/

  There is a role of tumor necrosis factor (TNF) and TNF receptors, as both are increased in this disease. This has been evidenced by the role of anti-TNF agents, such as pentoxifylline and infliximab. […] In addition to the T cell’s role, B cell hyperreactivity with immunoglobulin production is also implicated. Active sarcoidosis has also been associated with plasmatic hypergammaglobulinemia. Angiotensin-converting enzyme (ACE) levels correlated with elevated soluble HLA class I antigens levels in serum.

• #44 Sarcoidosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/301914-overview

  T cells play a central role in the development of sarcoidosis, as they likely propagate an excessive cellular immune reaction. For example, there is an accumulation of CD4 cells accompanied by the release of interleukin (IL)2 at sites of disease activity. This may manifest clinically by an inverted CD4/CD8 ratio. Pulmonary sarcoidosis is frequently characterized by a CD4+/CD8+ ratio of at least 3.5 in bronchoalveolar lavage fluid (BALF), although up to 40% of the cases present a normal or even decreased ratio, thus limiting its diagnostic value. Increased production of TH1 cytokines, such as interferon, is also a feature. […] Moreover, both tumor necrosis factor (TNF) and TNF receptors are increased in this disease. The importance of TNF in propagating inflammation in sarcoidosis has been demonstrated by the efficacy of anti-TNF agents, such as pentoxifylline and infliximab, in treating this disease.

• #45 Sarcoidosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK430687/

  There is a role of tumor necrosis factor (TNF) and TNF receptors, as both are increased in this disease. This has been evidenced by the role of anti-TNF agents, such as pentoxifylline and infliximab. […] In addition to the T cell’s role, B cell hyperreactivity with immunoglobulin production is also implicated. Active sarcoidosis has also been associated with plasmatic hypergammaglobulinemia. Angiotensin-converting enzyme (ACE) levels correlated with elevated soluble HLA class I antigens levels in serum.

• #46 Sarcoidosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/301914-overview

  T cells play a central role in the development of sarcoidosis, as they likely propagate an excessive cellular immune reaction. For example, there is an accumulation of CD4 cells accompanied by the release of interleukin (IL)2 at sites of disease activity. This may manifest clinically by an inverted CD4/CD8 ratio. Pulmonary sarcoidosis is frequently characterized by a CD4+/CD8+ ratio of at least 3.5 in bronchoalveolar lavage fluid (BALF), although up to 40% of the cases present a normal or even decreased ratio, thus limiting its diagnostic value. Increased production of TH1 cytokines, such as interferon, is also a feature. […] Moreover, both tumor necrosis factor (TNF) and TNF receptors are increased in this disease. The importance of TNF in propagating inflammation in sarcoidosis has been demonstrated by the efficacy of anti-TNF agents, such as pentoxifylline and infliximab, in treating this disease.

• #47 Psoriasiform Sarcoidosis Collision of Two Entities or Expression of One Common Pathogenesis? | JCAD – The Journal of Clinical and Aesthetic Dermatology

  https://jcadonline.com/psoriasiform-sarcoidosis-collision-of-two-entities-or-expression-of-one-common-pathogenesis/

  TNF-? is a critical component in the formation and maintenance of granulomas, and has a crucial role in the pathogenesis of psoriasis. […] The encouraging response to these biologic agents has emphasized the key role that TNF-? plays in the pathogenesis of sarcoidosis and possible immunopathogenic link for the development of psoriasiform sarcoidosis in patients with a psoriatic diathesis. […] The authors theorize that the co-expression of TNF-? in both entities may be an explanation for the development of psoriasiform lesions over plaques of sarcoidosis, such as seen in their patient.

• #48 Psoriasiform Sarcoidosis Collision of Two Entities or Expression of One Common Pathogenesis? | JCAD – The Journal of Clinical and Aesthetic Dermatology

  https://jcadonline.com/psoriasiform-sarcoidosis-collision-of-two-entities-or-expression-of-one-common-pathogenesis/

  TNF-? is a critical component in the formation and maintenance of granulomas, and has a crucial role in the pathogenesis of psoriasis. […] The encouraging response to these biologic agents has emphasized the key role that TNF-? plays in the pathogenesis of sarcoidosis and possible immunopathogenic link for the development of psoriasiform sarcoidosis in patients with a psoriatic diathesis. […] The authors theorize that the co-expression of TNF-? in both entities may be an explanation for the development of psoriasiform lesions over plaques of sarcoidosis, such as seen in their patient.

• #49 Sarcoidosis : Pathogenesis

  https://www.webpathology.com/images/hematopathology/lymph-node-non-hematopoietic/lymphadenopathies—i/38518

  Pathogenesis: Sarcoidosis is thought be the result of a dysfunctional cell-mediated immune response to unknown environmental antigens in genetically susceptible individuals. […] The process is driven by increased secretion of cytokines such as IL-2 (which lead to oligoclonal expansion of CD4+ helper T-cells) and IFN-gamma (which causes macrophage activation). […] Additional cytokines such as IL-8, TNF, and macrophage inflammatory protein 1-alpha attract additional lymphocytes and macrophages and lead to the formation of granulomas.

• #50 Sarcoidosis : Pathogenesis

  https://www.webpathology.com/images/hematopathology/lymph-node-non-hematopoietic/lymphadenopathies—i/38518

  Pathogenesis: Sarcoidosis is thought be the result of a dysfunctional cell-mediated immune response to unknown environmental antigens in genetically susceptible individuals. […] The process is driven by increased secretion of cytokines such as IL-2 (which lead to oligoclonal expansion of CD4+ helper T-cells) and IFN-gamma (which causes macrophage activation). […] Additional cytokines such as IL-8, TNF, and macrophage inflammatory protein 1-alpha attract additional lymphocytes and macrophages and lead to the formation of granulomas.

• #51

  https://link.springer.com/article/10.1186/s43556-025-00244-z

  The mTOR pathway plays an important role in pathogenesis of sarcoidosis. Activation of the mTORC1 signaling pathway occurs via signaling molecules such as IFN- and IL-17A, along with additional factors secreted by upstream Th1 and Th17 cells, facilitated through the JAK/STAT signaling pathway. […] The JAK protein family encompasses four distinct members: JAK1, JAK2, JAK3, and TYK2. In contrast, the STAT protein family consists of seven different members, namely STAT1, STAT2, STAT3, STAT4, STAT6, as well as STAT5A and STAT5B. IFN- can transduce signals via JAK1 and JAK2 to activate STAT1. […] The potential clinical significance of JAK inhibitors in the treatment of sarcoidosis is indicated by this finding. […] The molecular mechanisms and genetic predisposition discussed above provide several potential biomarkers that may be useful for sarcoidosis.

• #52

  https://link.springer.com/article/10.1186/s43556-025-00244-z

  The mTOR pathway plays an important role in pathogenesis of sarcoidosis. Activation of the mTORC1 signaling pathway occurs via signaling molecules such as IFN- and IL-17A, along with additional factors secreted by upstream Th1 and Th17 cells, facilitated through the JAK/STAT signaling pathway. […] The JAK protein family encompasses four distinct members: JAK1, JAK2, JAK3, and TYK2. In contrast, the STAT protein family consists of seven different members, namely STAT1, STAT2, STAT3, STAT4, STAT6, as well as STAT5A and STAT5B. IFN- can transduce signals via JAK1 and JAK2 to activate STAT1. […] The potential clinical significance of JAK inhibitors in the treatment of sarcoidosis is indicated by this finding. […] The molecular mechanisms and genetic predisposition discussed above provide several potential biomarkers that may be useful for sarcoidosis.

• #53

  https://link.springer.com/article/10.1186/s43556-025-00244-z

  The mTOR pathway plays an important role in pathogenesis of sarcoidosis. Activation of the mTORC1 signaling pathway occurs via signaling molecules such as IFN- and IL-17A, along with additional factors secreted by upstream Th1 and Th17 cells, facilitated through the JAK/STAT signaling pathway. […] The JAK protein family encompasses four distinct members: JAK1, JAK2, JAK3, and TYK2. In contrast, the STAT protein family consists of seven different members, namely STAT1, STAT2, STAT3, STAT4, STAT6, as well as STAT5A and STAT5B. IFN- can transduce signals via JAK1 and JAK2 to activate STAT1. […] The potential clinical significance of JAK inhibitors in the treatment of sarcoidosis is indicated by this finding. […] The molecular mechanisms and genetic predisposition discussed above provide several potential biomarkers that may be useful for sarcoidosis.

• #54 Sarcoidosis | Current concepts on pathogenesis, diagnosis and management of hepatic sarcoidosis | springermedicine.com

  https://www.springermedicine.com/sarcoidosis/sarcoidosis/current-concepts-on-pathogenesis-diagnosis-and-management-of-hep/50931908

  Sarcoidosis is an inflammatory multisystemic granulomatosis of unknown cause, with a wide range of clinical features, characterized by the presence of non-caseating granulomas. […] The immunopathogenesis of sarcoidosis is still unknown but it seems to involve the innate and adaptive immune actors in response to a putative antigen in genetically predisposed individuals. […] The NLRP3 inflammasome pathway is activated in sarcoidosis and involved in granuloma formation. […] The role of granulomatous phlebitis and thrombosis in the pathogenesis of cirrhosis and portal hypertension in sarcoidosis. […] Hepatic granulomas: pathogenesis and differential diagnosis.

• #55 Immunopathology of the Sarcoidosis | IntechOpen

  https://www.intechopen.com/chapters/82254

  Sarcoidosis as a multisystemic inflammatory granulomatous disorder is characterized by local immune hyperactivation, inflammation, and granuloma formation. […] The pathogenesis of sarcoidosis may be autoimmune response to an antigenic exposure. […] The immune mechanisms of sarcoidosis are not completely understood. The inflammasome signal transductions pathway plays a critical role in sarcoidosis pathogenesis. […] The exact pathogenesis of granuloma formation remains unknown. The cell-mediated delayed-type hypersensitivity immune reaction (type IV hypersensitivity) leads to granuloma formation in the context of immune dysfunction. […] The immune mechanisms of sarcoidosis are not completely understood. The inflammasome signal transductions pathway plays a critical role in sarcoidosis pathogenesis.

• #56 Sarcoidosis – Wikipedia

  https://en.wikipedia.org/wiki/Sarcoidosis

  The regulatory T-lymphocytes in the periphery of sarcoid granulomas appear to suppress IL-2 secretion, which is hypothesized to cause the state of anergy by preventing antigen-specific memory responses. […] While TNF is widely believed to play an important role in the formation of granulomas, sarcoidosis can and does still develop in those being treated with TNF antagonists like etanercept. […] B cells also likely play a role in the pathophysiology of sarcoidosis.

• #57 Sarcoidosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/301914-overview

  In addition to T cells, B cells also play a role. There is evidence of B cell hyperreactivity with immunoglobulin production. […] Soluble HLA class I antigens levels in serum and BALF are higher in patients with sarcoidosis. These levels tend to be significantly higher in active than in inactive stages and correlate with angiotensin-converting enzyme (ACE) levels. […] Active sarcoidosis has also been associated with plasmatic hypergammaglobulinemia. B-cell accumulation has been shown in pulmonary lesions, and a beneficial effect with anti-CD20 monoclonal antibody therapy has been reported in select patients. […] Glycoprotein KL-6 and surfactant protein D (SP-D) derived from alveolar type II cells and bronchiolar epithelial cells are significantly increased in pulmonary sarcoidosis and correlate with the percentage of lymphocytes in BALF, reflecting an inflammatory response in sarcoidosis. However, there is no significant correlation between KL-6 or SP-D levels and chest radiography findings, ACE levels, or CD4/CD8 ratio in BALF. KL-6 has been shown to be predictive of increased pulmonary parenchymal infiltration. […] A study by Facco et al suggests that Th17 cells may play a role in the pathogenesis and progression of sarcoidosis; these cells were noted to be present in the blood, BALF samples, and lung tissue from patients with sarcoidosis, particularly in those with the active form of the disease.

• #58 Sarcoidosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/301914-overview

  In addition to T cells, B cells also play a role. There is evidence of B cell hyperreactivity with immunoglobulin production. […] Soluble HLA class I antigens levels in serum and BALF are higher in patients with sarcoidosis. These levels tend to be significantly higher in active than in inactive stages and correlate with angiotensin-converting enzyme (ACE) levels. […] Active sarcoidosis has also been associated with plasmatic hypergammaglobulinemia. B-cell accumulation has been shown in pulmonary lesions, and a beneficial effect with anti-CD20 monoclonal antibody therapy has been reported in select patients. […] Glycoprotein KL-6 and surfactant protein D (SP-D) derived from alveolar type II cells and bronchiolar epithelial cells are significantly increased in pulmonary sarcoidosis and correlate with the percentage of lymphocytes in BALF, reflecting an inflammatory response in sarcoidosis. However, there is no significant correlation between KL-6 or SP-D levels and chest radiography findings, ACE levels, or CD4/CD8 ratio in BALF. KL-6 has been shown to be predictive of increased pulmonary parenchymal infiltration. […] A study by Facco et al suggests that Th17 cells may play a role in the pathogenesis and progression of sarcoidosis; these cells were noted to be present in the blood, BALF samples, and lung tissue from patients with sarcoidosis, particularly in those with the active form of the disease.

• #59 Sarcoidosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/301914-overview

  In addition to T cells, B cells also play a role. There is evidence of B cell hyperreactivity with immunoglobulin production. […] Soluble HLA class I antigens levels in serum and BALF are higher in patients with sarcoidosis. These levels tend to be significantly higher in active than in inactive stages and correlate with angiotensin-converting enzyme (ACE) levels. […] Active sarcoidosis has also been associated with plasmatic hypergammaglobulinemia. B-cell accumulation has been shown in pulmonary lesions, and a beneficial effect with anti-CD20 monoclonal antibody therapy has been reported in select patients. […] Glycoprotein KL-6 and surfactant protein D (SP-D) derived from alveolar type II cells and bronchiolar epithelial cells are significantly increased in pulmonary sarcoidosis and correlate with the percentage of lymphocytes in BALF, reflecting an inflammatory response in sarcoidosis. However, there is no significant correlation between KL-6 or SP-D levels and chest radiography findings, ACE levels, or CD4/CD8 ratio in BALF. KL-6 has been shown to be predictive of increased pulmonary parenchymal infiltration. […] A study by Facco et al suggests that Th17 cells may play a role in the pathogenesis and progression of sarcoidosis; these cells were noted to be present in the blood, BALF samples, and lung tissue from patients with sarcoidosis, particularly in those with the active form of the disease.

• #60 Sarcoidosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/301914-overview

  In addition to T cells, B cells also play a role. There is evidence of B cell hyperreactivity with immunoglobulin production. […] Soluble HLA class I antigens levels in serum and BALF are higher in patients with sarcoidosis. These levels tend to be significantly higher in active than in inactive stages and correlate with angiotensin-converting enzyme (ACE) levels. […] Active sarcoidosis has also been associated with plasmatic hypergammaglobulinemia. B-cell accumulation has been shown in pulmonary lesions, and a beneficial effect with anti-CD20 monoclonal antibody therapy has been reported in select patients. […] Glycoprotein KL-6 and surfactant protein D (SP-D) derived from alveolar type II cells and bronchiolar epithelial cells are significantly increased in pulmonary sarcoidosis and correlate with the percentage of lymphocytes in BALF, reflecting an inflammatory response in sarcoidosis. However, there is no significant correlation between KL-6 or SP-D levels and chest radiography findings, ACE levels, or CD4/CD8 ratio in BALF. KL-6 has been shown to be predictive of increased pulmonary parenchymal infiltration. […] A study by Facco et al suggests that Th17 cells may play a role in the pathogenesis and progression of sarcoidosis; these cells were noted to be present in the blood, BALF samples, and lung tissue from patients with sarcoidosis, particularly in those with the active form of the disease.

• #61 Sarcoidosis – Pulmonary Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/pulmonary-disorders/sarcoidosis/sarcoidosis

  Evidence supporting genetic susceptibility includes the following: Higher rate of disease concordance in monozygotic than dizygotic twins; Increased prevalence of sarcoidosis among first- or second-degree relatives of patients who have sarcoidosis; Marked increase in relative risk of developing sarcoidosis in siblings of patients who have sarcoidosis; Identification of several possible human leukocyte antigen (HLA) and non-HLA genes associated with sarcoidosis risk, course, and phenotypes. For example the HLA-DRB1*03/DQB1*02 haplotype is associated with Lfgren syndrome and predicts excellent prognosis, in contrast to HLA-DRB1*15/HLA DQB1*0602, which predicts persistent disease.

• #62

  https://www.medscape.org/viewarticle/466525

  Sarcoidosis is well known as a multisystem disease of unknown etiology characterized by the presence of noncaseating granuloma in affected organs. The etiology of sarcoidosis remains unknown and the disease remains a diagnosis of exclusion. The current understanding regarding the pathogenesis of the disease involves the exposure of a genetically susceptible individual to some environmental antigenic stimulus. […] Despite these efforts, the ability to identify a specific cause for this disease remains elusive. However, accumulating information regarding the underlying immunopathogenesis of sarcoidosis as well as the genetic contribution to this complex disease is ongoing. […] Evidence for a genetic predisposition to sarcoidosis derives from numerous sources. […] A study undertaken in white Spanish subjects demonstrated a prevalence in family contacts similar to the community. Conversely, a study evaluating African American and white subjects in Detroit found an increased prevalence of disease in family contacts compared with controls for the entire study cohort (13.5), which was greater in African Americans compared with white subjects (18.9:5.2).

• #63 Sarcoidosis – Pulmonary Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/pulmonary-disorders/sarcoidosis/sarcoidosis

  Evidence supporting genetic susceptibility includes the following: Higher rate of disease concordance in monozygotic than dizygotic twins; Increased prevalence of sarcoidosis among first- or second-degree relatives of patients who have sarcoidosis; Marked increase in relative risk of developing sarcoidosis in siblings of patients who have sarcoidosis; Identification of several possible human leukocyte antigen (HLA) and non-HLA genes associated with sarcoidosis risk, course, and phenotypes. For example the HLA-DRB1*03/DQB1*02 haplotype is associated with Lfgren syndrome and predicts excellent prognosis, in contrast to HLA-DRB1*15/HLA DQB1*0602, which predicts persistent disease.

• #64 Host-microbe interactions in the pathogenesis and clinical course of sarcoidosis | Journal of Biomedical Science | Full Text

  https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-019-0537-6

  Regulatory cells (Treg cells), which are defined as CD4+CD25brightFoxP3+ have been also implicated in the pathogenesis of sarcoidosis. […] The appearance of familiarly clustered cases of sarcoidosis and the racial differences in disease incidence and clinical progression support a possible link of genetics with the development of this disease. […] The most strongly and consistently associated risk factor for sarcoidosis is the major histocompatibility complex (MHC) region, comprising of HLA class I and class II genes, being HLA class II variants, particularly HLA-DRB1 and DQB1 the alleles most prevalently reported in association with sarcoidosis. […] Despite that numerous genetic risk factors in association with sarcoidosis have been identified, in the majority of cases, the biologic functions of specific variants and their precise interaction with environmental exposures remain unknown.

• #65 Sarcoidosis – Pulmonary Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/pulmonary-disorders/sarcoidosis/sarcoidosis

  Evidence supporting genetic susceptibility includes the following: Higher rate of disease concordance in monozygotic than dizygotic twins; Increased prevalence of sarcoidosis among first- or second-degree relatives of patients who have sarcoidosis; Marked increase in relative risk of developing sarcoidosis in siblings of patients who have sarcoidosis; Identification of several possible human leukocyte antigen (HLA) and non-HLA genes associated with sarcoidosis risk, course, and phenotypes. For example the HLA-DRB1*03/DQB1*02 haplotype is associated with Lfgren syndrome and predicts excellent prognosis, in contrast to HLA-DRB1*15/HLA DQB1*0602, which predicts persistent disease.

• #66 Neurosarcoidosis: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1147324-overview

  Tajima suggested a predominance of helper T cells in the sarcoid granulomas. Inflammation of the vasa nervorum or the arterioles to the muscles can result in ischemic injury or severe vasculitic neuropathy. […] A significantly higher prevalence of the HLA allele DQB1*0602 has been reported in sarcoidosis patients with small fiber neuropathy, and this allele has been associated with a severe course of disease. […] Peripheral nerve injury from these mechanisms may result in a diffuse polyneuropathy, mononeuritis multiplex, focal mononeuropathies, or polyradiculopathy from involvement of spinal root sheaths. The spinal root sheaths are an extension of the pachymeninges, a tissue for which sarcoid granulomas have a particular predilection.

• #67 Models Contribution to the Understanding of Sarcoidosis Pathogenesis: “Are There Good Models of Sarcoidosis?”

  https://www.mdpi.com/2077-0383/9/8/2445

  Models Contribution to the Understanding of Sarcoidosis Pathogenesis: “Are There Good Models of Sarcoidosis?” […] Sarcoidosis is a systemic, granulomatous, and noninfectious disease of unknown etiology. The clinical heterogeneity of the disease (targeted tissue(s), course of the disease, and therapy response) supports the idea that a multiplicity of trigger antigens may be involved. The pathogenesis of sarcoidosis is not yet completely understood, although in recent years, considerable efforts were put to develop novel experimental research models of sarcoidosis. […] The purpose of this review is to put in perspective the contributions of the most recent models in the understanding of sarcoidosis. […] Genetic susceptibility plays an important role in the pathogenesis of sarcoidosis. Recently, nucleotide-binding oligomerization domain 2 NOD2 mutations were involved in the pathogenesis of sarcoidosis, as well as in Blau syndrome (BS) and early onset sarcoidosis (EOS). […] A gene–environment interaction study identified additional genes (FCRL1, IL23R) that could distinguish patients with or without Löfgren’s syndrome.

• #68 Models Contribution to the Understanding of Sarcoidosis Pathogenesis: “Are There Good Models of Sarcoidosis?”

  https://www.mdpi.com/2077-0383/9/8/2445

  Models Contribution to the Understanding of Sarcoidosis Pathogenesis: “Are There Good Models of Sarcoidosis?” […] Sarcoidosis is a systemic, granulomatous, and noninfectious disease of unknown etiology. The clinical heterogeneity of the disease (targeted tissue(s), course of the disease, and therapy response) supports the idea that a multiplicity of trigger antigens may be involved. The pathogenesis of sarcoidosis is not yet completely understood, although in recent years, considerable efforts were put to develop novel experimental research models of sarcoidosis. […] The purpose of this review is to put in perspective the contributions of the most recent models in the understanding of sarcoidosis. […] Genetic susceptibility plays an important role in the pathogenesis of sarcoidosis. Recently, nucleotide-binding oligomerization domain 2 NOD2 mutations were involved in the pathogenesis of sarcoidosis, as well as in Blau syndrome (BS) and early onset sarcoidosis (EOS). […] A gene–environment interaction study identified additional genes (FCRL1, IL23R) that could distinguish patients with or without Löfgren’s syndrome.

• #69 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://www.mdpi.com/2077-0383/9/8/2363

  The involvement of both the innate and the adaptive immune cells calls into question the nature of the antigen/s involved in the pathogenesis of sarcoidosis. Thus far, apart from the tuberculin known to trigger the formation of the sarcoid granuloma, many have been the candidate antigens associated with the onset and the progression of the disease. Bacterial DNA has been identified in sarcoidosis lesions as well as autoantigens belonging to the major histocompatibility complex (MHC) class II molecules on antigen-presenting cells, recognized by the T-cell receptor (TCR) of the responding T-cells of sarcoidosis patients and leading to their clonal expansion. Strong T cell responses to vimentin, a peptide derived from the cytoskeleton, have been found in a subset of patients with sarcoidosis with a specific HLA type. Similarly, stimulation of peripheral blood mononuclear cells (PBMCs) from patients with sarcoidosis with vimentin triggers increased secretion of cytokines able to sustain the immune response, suggesting a self-perpetuating mechanism similar to that known to occur in autoimmune diseases. […] Overall, the immune cascade triggered by the antigen/s is much better known compared to the nature of the antigen itself. We here describe the role of innate and adaptive immune responses in the onset and the progression of sarcoidosis.

• #70 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://www.mdpi.com/2077-0383/9/8/2363

  The involvement of both the innate and the adaptive immune cells calls into question the nature of the antigen/s involved in the pathogenesis of sarcoidosis. Thus far, apart from the tuberculin known to trigger the formation of the sarcoid granuloma, many have been the candidate antigens associated with the onset and the progression of the disease. Bacterial DNA has been identified in sarcoidosis lesions as well as autoantigens belonging to the major histocompatibility complex (MHC) class II molecules on antigen-presenting cells, recognized by the T-cell receptor (TCR) of the responding T-cells of sarcoidosis patients and leading to their clonal expansion. Strong T cell responses to vimentin, a peptide derived from the cytoskeleton, have been found in a subset of patients with sarcoidosis with a specific HLA type. Similarly, stimulation of peripheral blood mononuclear cells (PBMCs) from patients with sarcoidosis with vimentin triggers increased secretion of cytokines able to sustain the immune response, suggesting a self-perpetuating mechanism similar to that known to occur in autoimmune diseases. […] Overall, the immune cascade triggered by the antigen/s is much better known compared to the nature of the antigen itself. We here describe the role of innate and adaptive immune responses in the onset and the progression of sarcoidosis.

• #71 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://www.mdpi.com/2077-0383/9/8/2363

  The involvement of both the innate and the adaptive immune cells calls into question the nature of the antigen/s involved in the pathogenesis of sarcoidosis. Thus far, apart from the tuberculin known to trigger the formation of the sarcoid granuloma, many have been the candidate antigens associated with the onset and the progression of the disease. Bacterial DNA has been identified in sarcoidosis lesions as well as autoantigens belonging to the major histocompatibility complex (MHC) class II molecules on antigen-presenting cells, recognized by the T-cell receptor (TCR) of the responding T-cells of sarcoidosis patients and leading to their clonal expansion. Strong T cell responses to vimentin, a peptide derived from the cytoskeleton, have been found in a subset of patients with sarcoidosis with a specific HLA type. Similarly, stimulation of peripheral blood mononuclear cells (PBMCs) from patients with sarcoidosis with vimentin triggers increased secretion of cytokines able to sustain the immune response, suggesting a self-perpetuating mechanism similar to that known to occur in autoimmune diseases. […] Overall, the immune cascade triggered by the antigen/s is much better known compared to the nature of the antigen itself. We here describe the role of innate and adaptive immune responses in the onset and the progression of sarcoidosis.

• #72 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://www.mdpi.com/2077-0383/9/8/2363

  The involvement of both the innate and the adaptive immune cells calls into question the nature of the antigen/s involved in the pathogenesis of sarcoidosis. Thus far, apart from the tuberculin known to trigger the formation of the sarcoid granuloma, many have been the candidate antigens associated with the onset and the progression of the disease. Bacterial DNA has been identified in sarcoidosis lesions as well as autoantigens belonging to the major histocompatibility complex (MHC) class II molecules on antigen-presenting cells, recognized by the T-cell receptor (TCR) of the responding T-cells of sarcoidosis patients and leading to their clonal expansion. Strong T cell responses to vimentin, a peptide derived from the cytoskeleton, have been found in a subset of patients with sarcoidosis with a specific HLA type. Similarly, stimulation of peripheral blood mononuclear cells (PBMCs) from patients with sarcoidosis with vimentin triggers increased secretion of cytokines able to sustain the immune response, suggesting a self-perpetuating mechanism similar to that known to occur in autoimmune diseases. […] Overall, the immune cascade triggered by the antigen/s is much better known compared to the nature of the antigen itself. We here describe the role of innate and adaptive immune responses in the onset and the progression of sarcoidosis.

• #73

  https://journals.lww.com/co-hematology/fulltext/2017/01000/mechanism_of_granuloma_formation_in_sarcoidosis.11.aspx

  The formation of noncaseating granuloma is a hallmark of pulmonary sarcoidosis. […] Compelling evidence exists that in acute but not chronic sarcoidosis CD4+ T lymphocytes specifically recognizing the auto-antigen vimentin on human leukocyte antigen-DR3 molecules accumulate in sarcoid granuloma. […] We provide a comprehensive update on the cellular components and their functional implications in sarcoid granuloma formation, with special emphasis on the specific characteristics of granuloma in acute versus chronic sarcoidosis.

• #74 Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art

  https://www.mdpi.com/2077-0383/9/8/2363

  The involvement of both the innate and the adaptive immune cells calls into question the nature of the antigen/s involved in the pathogenesis of sarcoidosis. Thus far, apart from the tuberculin known to trigger the formation of the sarcoid granuloma, many have been the candidate antigens associated with the onset and the progression of the disease. Bacterial DNA has been identified in sarcoidosis lesions as well as autoantigens belonging to the major histocompatibility complex (MHC) class II molecules on antigen-presenting cells, recognized by the T-cell receptor (TCR) of the responding T-cells of sarcoidosis patients and leading to their clonal expansion. Strong T cell responses to vimentin, a peptide derived from the cytoskeleton, have been found in a subset of patients with sarcoidosis with a specific HLA type. Similarly, stimulation of peripheral blood mononuclear cells (PBMCs) from patients with sarcoidosis with vimentin triggers increased secretion of cytokines able to sustain the immune response, suggesting a self-perpetuating mechanism similar to that known to occur in autoimmune diseases. […] Overall, the immune cascade triggered by the antigen/s is much better known compared to the nature of the antigen itself. We here describe the role of innate and adaptive immune responses in the onset and the progression of sarcoidosis.

• #75 Host-microbe interactions in the pathogenesis and clinical course of sarcoidosis | Journal of Biomedical Science | Full Text

  https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-019-0537-6

  Sarcoidosis has been also linked with certain environments factors such as exposure to inorganic particles, insecticides, and moldy environments. […] Taken together, the above discussed evidence appear to link mTB, other mycobacteria or their products with the excessive immune responses leading to sarcoidosis in a proportion of patients with sarcoidosis.

• #76 Host-microbe interactions in the pathogenesis and clinical course of sarcoidosis | Journal of Biomedical Science | Full Text

  https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-019-0537-6

  Sarcoidosis has been also linked with certain environments factors such as exposure to inorganic particles, insecticides, and moldy environments. […] Taken together, the above discussed evidence appear to link mTB, other mycobacteria or their products with the excessive immune responses leading to sarcoidosis in a proportion of patients with sarcoidosis.

• #77 Models Contribution to the Understanding of Sarcoidosis Pathogenesis: “Are There Good Models of Sarcoidosis?”

  https://www.mdpi.com/2077-0383/9/8/2445

  In vivo models were developed in mice exposed to putative sarcoidosis-causing agents, either antigens of infectious origin or inorganic particles. […] The two main in vivo models based on infectious agents followed different strategies: the use of mycobacterial antigens without provoking tuberculosis and the exposure to Cutibacterium acnes (C. acnes) (formerly named Propionibacterium acnes, P. acnes), which is a commensal strain of bacteria. […] The second model used C. acnes based on its detection in the lung and lymph nodes of patients. […] It can be emphasized that the various studies using C. acnes to induce pulmonary granulomatosis showed great variability concerning the mode of administration (sub-cutaneous, intravenous, intra-tracheal), the presence or not of adjuvant and the type of adjuvant used (incomplete Freund adjuvant, complete Freund adjuvant), the dose of C. acnes, the number of challenges, and the date of sacrifice.

• #78 Models Contribution to the Understanding of Sarcoidosis Pathogenesis: “Are There Good Models of Sarcoidosis?”

  https://www.mdpi.com/2077-0383/9/8/2445

  In vivo models were developed in mice exposed to putative sarcoidosis-causing agents, either antigens of infectious origin or inorganic particles. […] The two main in vivo models based on infectious agents followed different strategies: the use of mycobacterial antigens without provoking tuberculosis and the exposure to Cutibacterium acnes (C. acnes) (formerly named Propionibacterium acnes, P. acnes), which is a commensal strain of bacteria. […] The second model used C. acnes based on its detection in the lung and lymph nodes of patients. […] It can be emphasized that the various studies using C. acnes to induce pulmonary granulomatosis showed great variability concerning the mode of administration (sub-cutaneous, intravenous, intra-tracheal), the presence or not of adjuvant and the type of adjuvant used (incomplete Freund adjuvant, complete Freund adjuvant), the dose of C. acnes, the number of challenges, and the date of sacrifice.

• #79 Models Contribution to the Understanding of Sarcoidosis Pathogenesis: “Are There Good Models of Sarcoidosis?”

  https://www.mdpi.com/2077-0383/9/8/2445

  In vivo models were developed in mice exposed to putative sarcoidosis-causing agents, either antigens of infectious origin or inorganic particles. […] The two main in vivo models based on infectious agents followed different strategies: the use of mycobacterial antigens without provoking tuberculosis and the exposure to Cutibacterium acnes (C. acnes) (formerly named Propionibacterium acnes, P. acnes), which is a commensal strain of bacteria. […] The second model used C. acnes based on its detection in the lung and lymph nodes of patients. […] It can be emphasized that the various studies using C. acnes to induce pulmonary granulomatosis showed great variability concerning the mode of administration (sub-cutaneous, intravenous, intra-tracheal), the presence or not of adjuvant and the type of adjuvant used (incomplete Freund adjuvant, complete Freund adjuvant), the dose of C. acnes, the number of challenges, and the date of sacrifice.

• #80 Models Contribution to the Understanding of Sarcoidosis Pathogenesis: “Are There Good Models of Sarcoidosis?”

  https://www.mdpi.com/2077-0383/9/8/2445

  In vivo models were developed in mice exposed to putative sarcoidosis-causing agents, either antigens of infectious origin or inorganic particles. […] The two main in vivo models based on infectious agents followed different strategies: the use of mycobacterial antigens without provoking tuberculosis and the exposure to Cutibacterium acnes (C. acnes) (formerly named Propionibacterium acnes, P. acnes), which is a commensal strain of bacteria. […] The second model used C. acnes based on its detection in the lung and lymph nodes of patients. […] It can be emphasized that the various studies using C. acnes to induce pulmonary granulomatosis showed great variability concerning the mode of administration (sub-cutaneous, intravenous, intra-tracheal), the presence or not of adjuvant and the type of adjuvant used (incomplete Freund adjuvant, complete Freund adjuvant), the dose of C. acnes, the number of challenges, and the date of sacrifice.

• #81

  https://link.springer.com/article/10.1186/s43556-025-00244-z

  Sarcoidosis, a multisystemic granulomatous disease with unknown etiology, is characterized by formation of noncaseating granulomas, which can affect all organs. Recent studies have made outstanding achievement in understanding the pathology, etiology, genetics, and immune dysregulation involved in granuloma formation of sarcoidosis. […] The unresolved chronic inflammatory response is the key pathogenic mechanism underlying sarcoidosis, inducing irreversible organ dysfunctions. […] The main pathological mechanism of sarcoidosis involves antigen-presenting cells (such as macrophages and dendritic cells) that phagocytize antigens, leading to an abnormal immune response by CD4+T cells. This results in the secretion of inflammatory cytokines like IL-2 and IFN-, causing macrophage aggregation and fusion into granulomas.

• #82

  https://link.springer.com/article/10.1186/s43556-025-00244-z

  Sarcoidosis, a multisystemic granulomatous disease with unknown etiology, is characterized by formation of noncaseating granulomas, which can affect all organs. Recent studies have made outstanding achievement in understanding the pathology, etiology, genetics, and immune dysregulation involved in granuloma formation of sarcoidosis. […] The unresolved chronic inflammatory response is the key pathogenic mechanism underlying sarcoidosis, inducing irreversible organ dysfunctions. […] The main pathological mechanism of sarcoidosis involves antigen-presenting cells (such as macrophages and dendritic cells) that phagocytize antigens, leading to an abnormal immune response by CD4+T cells. This results in the secretion of inflammatory cytokines like IL-2 and IFN-, causing macrophage aggregation and fusion into granulomas.

• #83 Sarcoidosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/301914-overview

  In addition to T cells, B cells also play a role. There is evidence of B cell hyperreactivity with immunoglobulin production. […] Soluble HLA class I antigens levels in serum and BALF are higher in patients with sarcoidosis. These levels tend to be significantly higher in active than in inactive stages and correlate with angiotensin-converting enzyme (ACE) levels. […] Active sarcoidosis has also been associated with plasmatic hypergammaglobulinemia. B-cell accumulation has been shown in pulmonary lesions, and a beneficial effect with anti-CD20 monoclonal antibody therapy has been reported in select patients. […] Glycoprotein KL-6 and surfactant protein D (SP-D) derived from alveolar type II cells and bronchiolar epithelial cells are significantly increased in pulmonary sarcoidosis and correlate with the percentage of lymphocytes in BALF, reflecting an inflammatory response in sarcoidosis. However, there is no significant correlation between KL-6 or SP-D levels and chest radiography findings, ACE levels, or CD4/CD8 ratio in BALF. KL-6 has been shown to be predictive of increased pulmonary parenchymal infiltration. […] A study by Facco et al suggests that Th17 cells may play a role in the pathogenesis and progression of sarcoidosis; these cells were noted to be present in the blood, BALF samples, and lung tissue from patients with sarcoidosis, particularly in those with the active form of the disease.

• #84 Sarcoidosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/301914-overview

  In addition to T cells, B cells also play a role. There is evidence of B cell hyperreactivity with immunoglobulin production. […] Soluble HLA class I antigens levels in serum and BALF are higher in patients with sarcoidosis. These levels tend to be significantly higher in active than in inactive stages and correlate with angiotensin-converting enzyme (ACE) levels. […] Active sarcoidosis has also been associated with plasmatic hypergammaglobulinemia. B-cell accumulation has been shown in pulmonary lesions, and a beneficial effect with anti-CD20 monoclonal antibody therapy has been reported in select patients. […] Glycoprotein KL-6 and surfactant protein D (SP-D) derived from alveolar type II cells and bronchiolar epithelial cells are significantly increased in pulmonary sarcoidosis and correlate with the percentage of lymphocytes in BALF, reflecting an inflammatory response in sarcoidosis. However, there is no significant correlation between KL-6 or SP-D levels and chest radiography findings, ACE levels, or CD4/CD8 ratio in BALF. KL-6 has been shown to be predictive of increased pulmonary parenchymal infiltration. […] A study by Facco et al suggests that Th17 cells may play a role in the pathogenesis and progression of sarcoidosis; these cells were noted to be present in the blood, BALF samples, and lung tissue from patients with sarcoidosis, particularly in those with the active form of the disease.

• #85 A clinical overview of sarcoidosis: Pathogenesis symptoms diagnosis and treatment – Journal of Translational Medical Research

  https://journal.bums.ac.ir/article-1-3338-en.html

  Sarcoidosis is a granulomatous disorder characterized by non-caseating granulomas in multiple organs and an unknown cause. […] Although its aetiology is not well understood, there are indications of the genetic basis and the involvement of specific microorganisms and vitamin D in the development of this disease. […] Future research should focus on the combination of biomarkers and more refined imaging techniques, such as computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET). […] By utilizing these techniques and markers, it may be possible to design diagnostic and therapeutic approaches. […] Serum B cell activating factor (BAFF) and sarcoidosis activity. […] Clinically-useful serum biomarkers for diagnosis and prognosis of sarcoidosis. […] Biomarkers in the Diagnosis and Prognosis of Sarcoidosis: Current Use and Future Prospects. […] Etiologies of sarcoidosis.

• #86 A clinical overview of sarcoidosis: Pathogenesis symptoms diagnosis and treatment – Journal of Translational Medical Research

  https://journal.bums.ac.ir/article-1-3338-en.html

  Sarcoidosis is a granulomatous disorder characterized by non-caseating granulomas in multiple organs and an unknown cause. […] Although its aetiology is not well understood, there are indications of the genetic basis and the involvement of specific microorganisms and vitamin D in the development of this disease. […] Future research should focus on the combination of biomarkers and more refined imaging techniques, such as computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET). […] By utilizing these techniques and markers, it may be possible to design diagnostic and therapeutic approaches. […] Serum B cell activating factor (BAFF) and sarcoidosis activity. […] Clinically-useful serum biomarkers for diagnosis and prognosis of sarcoidosis. […] Biomarkers in the Diagnosis and Prognosis of Sarcoidosis: Current Use and Future Prospects. […] Etiologies of sarcoidosis.

• #87 Sarcoidosis | Nature Reviews Disease Primers

  https://www.nature.com/articles/s41572-019-0096-x

  Sarcoidosis is an inflammatory disorder of unknown cause that is characterized by granuloma formation in affected organs, most often in the lungs. […] The typical T cell accumulation, local T cell immune response and granuloma formation in the lungs indicate that the inflammatory response in sarcoidosis is induced by specific antigens, possibly including self-antigens, which is consistent with an autoimmune involvement. […] As the aetiology of sarcoidosis is unknown, no specific treatment and no pathognomic markers exist. […] Thus, improved biomarkers to determine disease activity and to identify patients at risk of developing fibrosis are needed. […] Corticosteroids still constitute the first-line treatment, but new treatment strategies, including those targeting quality-of-life issues, are being evaluated and should yield appropriate, personalized and more effective treatments.

• #88 Immunopathology of the Sarcoidosis | IntechOpen

  https://www.intechopen.com/chapters/82254

  The genetic predisposition concept to sarcoidosis susceptibility and the causative antigen nature had not been well defined. […] Corticosteroids are the first-line therapeutic approach due to potent anti-inflammatory and immune-suppressing actions, which inhibit TNF-, INF-, and related (e.g. NF-B) signaling pathways. […] The most useful approach to simultaneously diagnose, treat, and predict prognosis in sarcoidosis may be to measure immune system biomarkers in blood or BAL fluid panel. […] Therefore, sarcoidosis treatment could potentially benefit from simultaneous modulation and fine-tuning of M2/Th2 and M1/Th1 pathways rather than targeting one pathway or the other.

• #89

  https://link.springer.com/article/10.1186/s43556-025-00244-z

  Recent studies have found that the pathological mechanisms of sarcoidosis also involve other pro-inflammatory factors (such as TNF-) and multiple signaling pathways (such as mTOR and JAK-STAT pathway). These findings suggest new promising therapeutic targets for sarcoidosis. […] Given the unknown etiology of this granulomatous disease, sarcoidosis cannot be categorized as an autoimmune disorder. However, certain studies have indicated that immune disorders significantly contribute to the development of sarcoidosis. […] The elucidation of the autoimmunity mechanism in sarcoidosis can enable the application of targeted immunotherapy and aid in the identification of key biomarkers in patients with sarcoidosis. […] The granulomatous response in sarcoidosis is triggered by the three-component complex of T-cell receptor (TCR)-peptide-HLA, serving as the initial stimulatory signal for antigen-specific T cells, followed by stimulation from co-stimulatory molecules as a second signal.

• #90 About Pulmonary Sarcoidosis – aTyr Pharma

  https://atyrpharma.com/patients/about-pulmonary-sarcoidosis/

  Sarcoidosis is an inflammatory disease characterized by the formation of granulomas, clumps of inflammatory cells, in one or more organs in the body. […] The pathogenesis of sarcoidosis is not yet well understood. A leading hypothesis is that granuloma formation involves the interplay between antigen, human leukocyte antigen (HLA) class II molecules, and T-cell receptors: a presumptive sarcoid antigen is engulfed by circulating antigen-presenting cells (APCs: macrophages, dendritic cells) and the subsequent interplay between APCs and CD4+ T-cells initiates granuloma formation. T lymphocyte activation subsequently plays a crucial role in sarcoidosis pathogenesis. […] Moreover, the mechanism of action of efzofitimod in T-cells and macrophages potentially overlaps with the cellular pathology observed in pulmonary sarcoidosis. In preclinical studies, efzofitimod has been observed to attenuate T-cell activation and inhibit cytokines and chemokines involved in regulation of inflammatory responses, while also modulating macrophage endosome maturation. […] We have also shown that the active portion of efzofitimod has the ability to disrupt sarcoid granuloma formation in vitro.

• #91 About Pulmonary Sarcoidosis – aTyr Pharma

  https://atyrpharma.com/patients/about-pulmonary-sarcoidosis/

  Sarcoidosis is an inflammatory disease characterized by the formation of granulomas, clumps of inflammatory cells, in one or more organs in the body. […] The pathogenesis of sarcoidosis is not yet well understood. A leading hypothesis is that granuloma formation involves the interplay between antigen, human leukocyte antigen (HLA) class II molecules, and T-cell receptors: a presumptive sarcoid antigen is engulfed by circulating antigen-presenting cells (APCs: macrophages, dendritic cells) and the subsequent interplay between APCs and CD4+ T-cells initiates granuloma formation. T lymphocyte activation subsequently plays a crucial role in sarcoidosis pathogenesis. […] Moreover, the mechanism of action of efzofitimod in T-cells and macrophages potentially overlaps with the cellular pathology observed in pulmonary sarcoidosis. In preclinical studies, efzofitimod has been observed to attenuate T-cell activation and inhibit cytokines and chemokines involved in regulation of inflammatory responses, while also modulating macrophage endosome maturation. […] We have also shown that the active portion of efzofitimod has the ability to disrupt sarcoid granuloma formation in vitro.

• #92 About Pulmonary Sarcoidosis – aTyr Pharma

  https://atyrpharma.com/patients/about-pulmonary-sarcoidosis/

  Sarcoidosis is an inflammatory disease characterized by the formation of granulomas, clumps of inflammatory cells, in one or more organs in the body. […] The pathogenesis of sarcoidosis is not yet well understood. A leading hypothesis is that granuloma formation involves the interplay between antigen, human leukocyte antigen (HLA) class II molecules, and T-cell receptors: a presumptive sarcoid antigen is engulfed by circulating antigen-presenting cells (APCs: macrophages, dendritic cells) and the subsequent interplay between APCs and CD4+ T-cells initiates granuloma formation. T lymphocyte activation subsequently plays a crucial role in sarcoidosis pathogenesis. […] Moreover, the mechanism of action of efzofitimod in T-cells and macrophages potentially overlaps with the cellular pathology observed in pulmonary sarcoidosis. In preclinical studies, efzofitimod has been observed to attenuate T-cell activation and inhibit cytokines and chemokines involved in regulation of inflammatory responses, while also modulating macrophage endosome maturation. […] We have also shown that the active portion of efzofitimod has the ability to disrupt sarcoid granuloma formation in vitro.

• #93 SciELO Brazil – Sarcoidosis: a general overview Sarcoidosis: a general overview

  https://www.scielo.br/j/adr/a/8CpXmPpVVqm65bhz85Z9VbP/

  An interesting hypothesis is that the granulomatous response persists as long as there is insufficient clearance of the causative antigen, and throughout this period it causes different symptoms to the patient (it could explain the habitual self-limited course of the disease). In this hypothesis, the entry of the causative antigens is possibly via inhalation, an idea that can be deduced from the fact that almost all cases of sarcoidosis begin with pulmonary involvement and mediastinal lymphadenopathy. Biopsies of organs affected by sarcoidosis reveal multiple granulomas, which consist of clusters of multinucleated giant cells and epithelioid cells, organized in a round shape, surrounded by lymphocytes. Staining for infectious agents (at least mycobacteria and fungi) must be negative. In the center of these granulomas there is generally no necrosis. For this reason, they are usually described as noncaseating granulomas, as opposed to the granuloma typical of infectious diseases, which often reveals extensive necrotic areas in its center, presenting a macroscopic cheese-like (caseating) appearance. However, mature granulomas in sarcoidosis also may present central areas of fibrinoid necrosis, and there are reports of extensive necrosis in sarcoid granulomas described as caseating in some areas. Thus the finding of necrosis or even some caseum at biopsy is not sufficient to rule out the diagnosis of sarcoidosis.

• #94 SciELO Brazil – Sarcoidosis: a general overview Sarcoidosis: a general overview

  https://www.scielo.br/j/adr/a/8CpXmPpVVqm65bhz85Z9VbP/

  An interesting hypothesis is that the granulomatous response persists as long as there is insufficient clearance of the causative antigen, and throughout this period it causes different symptoms to the patient (it could explain the habitual self-limited course of the disease). In this hypothesis, the entry of the causative antigens is possibly via inhalation, an idea that can be deduced from the fact that almost all cases of sarcoidosis begin with pulmonary involvement and mediastinal lymphadenopathy. Biopsies of organs affected by sarcoidosis reveal multiple granulomas, which consist of clusters of multinucleated giant cells and epithelioid cells, organized in a round shape, surrounded by lymphocytes. Staining for infectious agents (at least mycobacteria and fungi) must be negative. In the center of these granulomas there is generally no necrosis. For this reason, they are usually described as noncaseating granulomas, as opposed to the granuloma typical of infectious diseases, which often reveals extensive necrotic areas in its center, presenting a macroscopic cheese-like (caseating) appearance. However, mature granulomas in sarcoidosis also may present central areas of fibrinoid necrosis, and there are reports of extensive necrosis in sarcoid granulomas described as caseating in some areas. Thus the finding of necrosis or even some caseum at biopsy is not sufficient to rule out the diagnosis of sarcoidosis.

• #95 SciELO Brazil – Sarcoidosis: a general overview Sarcoidosis: a general overview

  https://www.scielo.br/j/adr/a/8CpXmPpVVqm65bhz85Z9VbP/

  Like many other idiopathic inflammatory diseases, sarcoidosis is believed to occur in individuals with certain genetic predispositions after exposure to environmental triggers. However, both factors are essentially unknown. Sarcoidosis is associated with some human leukocyte antigens (HLA) class II alleles, but not with a specific genetic variant. In granulomatous lesions of sarcoidosis, different microbial DNA was found, but viable microorganisms were never observed. Also exposure to inorganic dusts and immunoreactivity against these compounds are associated with sarcoidosis. Therefore, sarcoidosis is neither a genetic nor an infectious disease; it is probably a disease that arises in individuals who develop an inappropriate immune response when challenged by certain infectious or inorganic antigens. This inappropriate immune response is based on the Th1 and Th17 pathways and induces the granulomatous inflammatory process typical of sarcoidosis, in which tumour necrosis fator alpha (TNFa) produced by activated macrophages has a fundamental role.

• #96 Introductory Chapter: Sarcoidosis – New Perspectives | IntechOpen

  https://www.intechopen.com/chapters/82125

  Autoimmunity presents a novel spectrum for immunopathogenesis of sarcoidosis and may help elucidate sarcoid etiology. […] Despite extensive research over the past several decades, the sarcoidosis etiology remained unknown. […] The integration of the recent deep data will allow to fill the gap between genotype and phenotype, avoiding false-negative and false-positive results. […] For better disease management, multifaceted approaches remain the best practice to ensure competent and effective patient care.

• #97 Introductory Chapter: Sarcoidosis – New Perspectives | IntechOpen

  https://www.intechopen.com/chapters/82125

  Autoimmunity presents a novel spectrum for immunopathogenesis of sarcoidosis and may help elucidate sarcoid etiology. […] Despite extensive research over the past several decades, the sarcoidosis etiology remained unknown. […] The integration of the recent deep data will allow to fill the gap between genotype and phenotype, avoiding false-negative and false-positive results. […] For better disease management, multifaceted approaches remain the best practice to ensure competent and effective patient care.

• #98 Introductory Chapter: Sarcoidosis – New Perspectives | IntechOpen

  https://www.intechopen.com/chapters/82125

  Autoimmunity presents a novel spectrum for immunopathogenesis of sarcoidosis and may help elucidate sarcoid etiology. […] Despite extensive research over the past several decades, the sarcoidosis etiology remained unknown. […] The integration of the recent deep data will allow to fill the gap between genotype and phenotype, avoiding false-negative and false-positive results. […] For better disease management, multifaceted approaches remain the best practice to ensure competent and effective patient care.

• #99 Silicosarcoidosis: Researchers coin new term to define distinct occupational lung disease

  https://medicalxpress.com/news/2025-05-silicosarcoidosis-coin-term-distinct-occupational.html

  In a study led by a multinational team of experts, researchers at National Jewish Health and their collaborators in Colorado, Illinois, Taiwan and Israel have introduced a new term to the medical lexicon: silicosarcoidosis. This novel designation describes cases where patients’ lung tissue exhibits overlapping features of both silicosis and sarcoidosis, two serious pulmonary diseases linked to occupational exposure to respirable crystalline silica (RCS) commonly found in construction, mining, and engineered stone fabrication. […] Sarcoidosis, a systemic inflammatory condition of unknown origin, is increasingly being linked to environmental and occupational exposures. However, exposure histories are rarely sought during clinical evaluation. The study’s authors argue that the term silicosarcoidosis can help bridge this gap by acknowledging silica exposure as a significant and modifiable risk factor in some patients with sarcoidosis.

• #100 Silicosarcoidosis: Researchers coin new term to define distinct occupational lung disease

  https://medicalxpress.com/news/2025-05-silicosarcoidosis-coin-term-distinct-occupational.html

  In a study led by a multinational team of experts, researchers at National Jewish Health and their collaborators in Colorado, Illinois, Taiwan and Israel have introduced a new term to the medical lexicon: silicosarcoidosis. This novel designation describes cases where patients’ lung tissue exhibits overlapping features of both silicosis and sarcoidosis, two serious pulmonary diseases linked to occupational exposure to respirable crystalline silica (RCS) commonly found in construction, mining, and engineered stone fabrication. […] Sarcoidosis, a systemic inflammatory condition of unknown origin, is increasingly being linked to environmental and occupational exposures. However, exposure histories are rarely sought during clinical evaluation. The study’s authors argue that the term silicosarcoidosis can help bridge this gap by acknowledging silica exposure as a significant and modifiable risk factor in some patients with sarcoidosis.

• #101 Silicosarcoidosis: Researchers coin new term to define distinct occupational lung disease

  https://medicalxpress.com/news/2025-05-silicosarcoidosis-coin-term-distinct-occupational.html

  In a study led by a multinational team of experts, researchers at National Jewish Health and their collaborators in Colorado, Illinois, Taiwan and Israel have introduced a new term to the medical lexicon: silicosarcoidosis. This novel designation describes cases where patients’ lung tissue exhibits overlapping features of both silicosis and sarcoidosis, two serious pulmonary diseases linked to occupational exposure to respirable crystalline silica (RCS) commonly found in construction, mining, and engineered stone fabrication. […] Sarcoidosis, a systemic inflammatory condition of unknown origin, is increasingly being linked to environmental and occupational exposures. However, exposure histories are rarely sought during clinical evaluation. The study’s authors argue that the term silicosarcoidosis can help bridge this gap by acknowledging silica exposure as a significant and modifiable risk factor in some patients with sarcoidosis.

• #102 Silicosarcoidosis: Researchers coin new term to define distinct occupational lung disease

  https://medicalxpress.com/news/2025-05-silicosarcoidosis-coin-term-distinct-occupational.html

  A quantitative microscopy technique developed by Dr. Hua’s research team measured significantly elevated dust particle densities in lung tissue, confirming the overabundance of silica compared to healthy controls. […] „This study brings much-needed clarity to the overlap between two complex lung diseases and reaffirms the critical role of an exposure history in pulmonary diagnosis,” said Cecile Rose, MD, senior author of the study and occupational pulmonologist at National Jewish Health. […] „The introduction of 'silicosarcoidosis’ marks a pivotal step in considering both treatment approaches and preventive strategies, especially in pulmonary clinical practice.”

• #103 Silicosarcoidosis: Researchers coin new term to define distinct occupational lung disease

  https://medicalxpress.com/news/2025-05-silicosarcoidosis-coin-term-distinct-occupational.html

  A quantitative microscopy technique developed by Dr. Hua’s research team measured significantly elevated dust particle densities in lung tissue, confirming the overabundance of silica compared to healthy controls. […] „This study brings much-needed clarity to the overlap between two complex lung diseases and reaffirms the critical role of an exposure history in pulmonary diagnosis,” said Cecile Rose, MD, senior author of the study and occupational pulmonologist at National Jewish Health. […] „The introduction of 'silicosarcoidosis’ marks a pivotal step in considering both treatment approaches and preventive strategies, especially in pulmonary clinical practice.”

• #104 Silicosarcoidosis: Researchers coin new term to define distinct occupational lung disease

  https://medicalxpress.com/news/2025-05-silicosarcoidosis-coin-term-distinct-occupational.html

  A quantitative microscopy technique developed by Dr. Hua’s research team measured significantly elevated dust particle densities in lung tissue, confirming the overabundance of silica compared to healthy controls. […] „This study brings much-needed clarity to the overlap between two complex lung diseases and reaffirms the critical role of an exposure history in pulmonary diagnosis,” said Cecile Rose, MD, senior author of the study and occupational pulmonologist at National Jewish Health. […] „The introduction of 'silicosarcoidosis’ marks a pivotal step in considering both treatment approaches and preventive strategies, especially in pulmonary clinical practice.”

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