2016
DOI: 10.1111/1346-8138.13186
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Psoriasis: Behind the scenes

Abstract: Psoriasis is a chronic inflammatory skin disease characterized by a significant deterioration in the quality of life of affected individuals. Notably, psoriasis is significantly associated with cardiovascular and metabolic syndrome and other autoimmune disorders. Recent progress in biologic therapies has revealed the fundamental role of tumor necrosis factor-a, interleukin (IL)-23 and the IL-17A axis together with aberrant overproduction of epidermal IL-36c in the pathogenesis of psoriasis. This review provide… Show more

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Cited by 29 publications
(22 citation statements)
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References 90 publications
(210 reference statements)
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“…In addition, recent therapeutic success with other biologics seems to have revealed the pivotal role of the TNF-α/interleukin (IL)-23/IL-17 axis in the pathogenesis of psoriasis (Figure). The initial trigger of psoriasis is thought to be the activation of plasmacytoid dendritic cells (DCs) being stimulated by complexes of host DNA and the antimicrobial peptide LL-37 (cathelicidin), which are produced by keratinocytes after minor injuries (8, 13-15). Activated plasmacytoid DCs and damaged keratinocytes produce interferon (IFN)-α and TNF-α, which results in the further production of TNF-α, IL-12 and IL-23 by plasmacytoids and recruited inflammatory DCs (8, 14, 15) (Figure).…”
Section: Pathogenesis Of Psoriasismentioning
confidence: 99%
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“…In addition, recent therapeutic success with other biologics seems to have revealed the pivotal role of the TNF-α/interleukin (IL)-23/IL-17 axis in the pathogenesis of psoriasis (Figure). The initial trigger of psoriasis is thought to be the activation of plasmacytoid dendritic cells (DCs) being stimulated by complexes of host DNA and the antimicrobial peptide LL-37 (cathelicidin), which are produced by keratinocytes after minor injuries (8, 13-15). Activated plasmacytoid DCs and damaged keratinocytes produce interferon (IFN)-α and TNF-α, which results in the further production of TNF-α, IL-12 and IL-23 by plasmacytoids and recruited inflammatory DCs (8, 14, 15) (Figure).…”
Section: Pathogenesis Of Psoriasismentioning
confidence: 99%
“…In humans and experimental models of psoriasis, γδT cells (Vγ9Vδ2 T cells in human), innate lymphoid cells type 3 (ILC3) and Th17 cells are detected in blood and lesional skin. These cells readily produce IL-17A and IL-22 (8, 17, 18). IL-17A binds to the IL-17 receptor (IL-17R), which is composed of IL-17RA and IL-17RC (19) (Figure).…”
Section: Pathogenesis Of Psoriasismentioning
confidence: 99%
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