The role of interleukin-17 in the pathogenesis of systemic sclerosis: Pro-fibrotic or anti-fibrotic?. Issue 3 (October 2021)

• Record Type: Journal Article
• Authors: Bellando-Randone, Silvia; Della-Torre, Emanuel; Balanescu, Andra
• Is Part Of: Journal of scleroderma and related disorders. Volume 6:Issue 3(2021)
• Page Start: 227
• Page End: 235
• Publication Date: 2021-10
• Subjects: Systemic sclerosis -- interleukin-17 -- fibrosis -- T helper 17 -- fibroblast; Scleroderma (Disease) -- Periodicals; Systemic scleroderma -- Periodicals; Fibrosis -- Periodicals; 616.544
• DOI: 10.1177/23971983211039421
• Languages: English
• ISSNs: 2397-1983

Abstract

Systemic sclerosis is characterized by widespread fibrosis of the skin and internal organs, vascular impairment, and dysregulation of innate and adaptive immune system. Growing evidence indicates that T-cell proliferation and cytokine secretion play a major role in the initiation of systemic sclerosis, but the role of T helper 17 cells and of interleukin-17 cytokines in the development and progression of the disease remains controversial. In particular, an equally distributed body of literature supports both pro-fibrotic and anti-fibrotic effects of interleukin-17, suggesting a complex and nuanced role of this cytokine in systemic sclerosis pathogenesis that may vary depending on disease stage, target cells in affected organs, and inflammatory milieu. Although interleukin-17 already represents an established therapeutic target for several immune-mediated inflammatory diseases, more robust experimental evidence is required to clarify whether it may become an attractive therapeutic target for systemic sclerosis as well.