2020
DOI: 10.1007/s12026-020-09149-1
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The role of Th17 cells in psoriasis

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Cited by 88 publications
(74 citation statements)
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References 165 publications
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“…However, serum analysis from psoriatic individuals has indicated antibodies against Malassezia and its antigens (Squiquera et al, 1994;Gemmer et al, 2002;Jagielski et al, 2014). In Psoriasis, interleukin 23 (IL-23)/Th17 immune axis has been identified as a major pathway (Blauvelt, 2008;Girolomoni et al, 2017;Li et al, 2020). Malassezia can also induce Th1-related cytokines in peripheral blood mononuclear cells in vitro (Kanda et al, 2002;Valli et al, 2010) and induce keratinocyte proliferation and proinflammatory cytokine production which could potentially enhance inflammation (Baroni et al, 2004).…”
Section: Malassezia In Atopic Dermatitis: Pathogenesis or Mutualism?mentioning
confidence: 99%
“…However, serum analysis from psoriatic individuals has indicated antibodies against Malassezia and its antigens (Squiquera et al, 1994;Gemmer et al, 2002;Jagielski et al, 2014). In Psoriasis, interleukin 23 (IL-23)/Th17 immune axis has been identified as a major pathway (Blauvelt, 2008;Girolomoni et al, 2017;Li et al, 2020). Malassezia can also induce Th1-related cytokines in peripheral blood mononuclear cells in vitro (Kanda et al, 2002;Valli et al, 2010) and induce keratinocyte proliferation and proinflammatory cytokine production which could potentially enhance inflammation (Baroni et al, 2004).…”
Section: Malassezia In Atopic Dermatitis: Pathogenesis or Mutualism?mentioning
confidence: 99%
“…Patients on systemic treatments have more severe psoriasis, with increased initial PASI scores and recalcitrance to exclusive topical treatments. It is known that Th17 inflammatory axis activation has a positive correlation with the severity of psoriasis [ 9 ]. This fact explains the higher detection of IL-17A in G1, G2 and G4, which was not seen in the topical treatment group (G3) with mild psoriasis.…”
Section: Discussionmentioning
confidence: 99%
“…This analysis represents the first step in the comprehension of innate and adaptative immune responses against viral infections in a population with an imbalanced immune system. Psoriasis, like many other inflammatory and autoimmune diseases—such as multiple sclerosis, rheumatoid arthritis and inflammatory bowel disease—presents a deviation of T lymphocytes to a Th17 pattern [ 9 ]. Although the IL-23/Th-17 pathway leads to the production of anti-viral cytokines in the skin of psoriatic patients (type III IFN) [ 2 , 7 ], it is still unknown whether these molecules play an important role in the prevention of systemic infections, such as COVID-19.…”
Section: Discussionmentioning
confidence: 99%
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“…Inflammatory diseases such as rheumatoid arthritis, psoriasis, and inflammatory bowel disease are sometimes exacerbated by lymphocytes [14][15][16][17]. IL-17-producing cells are related to inflammation induced by the synergistic effect of certain inflammatory cytokines, including IL-23 and TNF-α, and antigen-presenting cells, following the upregulation of transcription factor RORγt [18]. In the development of IL-17-producing CD4 + cells, TGF-β and IL-6 are required for the differentiation from naïve T cells [19].…”
Section: Th17 Cells and Antimicrobial Action Against Fungimentioning
confidence: 99%