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Digestive Diseases and Sciences

Erschienen in:

02.03.2020 | INVITED REVIEW

Controversial Contribution of Th17/IL-17 Toward the Immune Response in Intestinal Fibrosis

verfasst von: Giovanni Latella, Angelo Viscido

Erschienen in: Digestive Diseases and Sciences | Ausgabe 5/2020

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Abstract

Intestinal fibrosis is a common outcome of inflammatory bowel diseases (IBDs), becoming clinically apparent in 40% of patients with Crohn’s disease and 5% of those with ulcerative colitis. Effective pharmacological treatments aimed at controlling or reversing fibrosis progression are unavailable. Fibrosis is characterized by an excessive local accumulation of extracellular matrix proteins (mainly collagen), as a result of their increased production by activated myofibroblasts and/or their reduced degradation by specific matrix metalloproteinases. Initiation and progression of fibrosis are modulated by several pro- and anti-fibrogenic molecules. In recent years, the cytokine interleukin-17 (IL-17) has been integrated into the pathogenesis of fibrosis, although its precise contribution to IBD, and especially to its related intestinal fibrosis, remains controversial. Several data suggest both a pro-inflammatory and pro-fibrotic action and a protective function of the Th17/IL-17 immune response. A recent study has demonstrated that the treatment with anti-IL-17 antibody significantly alleviated 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colorectal fibrosis in mice by down-regulating the expression of collagen 3 and several pro-fibrogenic cytokines. Here, we describe and discuss the possible involvement of the Th17/IL-17 immune response in the initiation ad progression of intestinal fibrosis.

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Titel: Controversial Contribution of Th17/IL-17 Toward the Immune Response in Intestinal Fibrosis
verfasst von: Giovanni Latella
Angelo Viscido
Publikationsdatum: 02.03.2020
Verlag: Springer US
Erschienen in: Digestive Diseases and Sciences / Ausgabe 5/2020
Print ISSN: 0163-2116
Elektronische ISSN: 1573-2568
DOI: https://doi.org/10.1007/s10620-020-06161-1

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