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Review ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Immunol. | doi: 10.3389/fimmu.2019.02025

The roles of IL-1 family cytokines in the pathogenesis of systemic sclerosis

 Dan Xu1 and Rong Mu1*
  • 1Department of Rheumatology & Immunology, Peking University People’s Hospital, China

The IL-1 family consists of 11 cytokines, 7 ligands with agonist activity (IL-1𝛼, IL-1𝛽, IL-18, IL-33, IL-36𝛼, IL-36𝛽, IL-36𝛾) and 4 members with antagonistic activities (IL-1 receptor antagonist (IL-1Ra), IL-36Ra, IL-37, IL-38). Recent articles have described that most members of IL-1 family cytokines are involved in the process of innate and adaptive immunity as well as fibrosis in systemic sclerosis (SSc). IL-1 family gene polymorphisms, abnormal expression of IL-1 and its potential role in the fibrosis process have been explored in SSc. IL-33 and IL-18 have also been discussed in the recent years. IL-33 may contribute to the fibrosis of SSc, while IL-18 remains to be researched to confirm its role in fibrosis process. There is a lack of study on the pathophysiological roles of IL-36, IL-37 and IL-38 in SSc, which might provide us new study area. Here, we aim to give a brief overview of IL-1 family cytokines and discuss their pivotal roles in the pathogenesis of SSc.

Keywords: IL-1 family cytokines, systemic sclerosis, scleroderma, Fibrosis, Pathogenesis

Received: 31 Jan 2019; Accepted: 09 Aug 2019.

Copyright: © 2019 Xu and Mu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Rong Mu, Department of Rheumatology & Immunology, Peking University People’s Hospital, Beijing, China,