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Interleukin‐35 regulates the balance of Th17 and Treg responses during the pathogenesis of connective tissue diseases
Author(s) -
Wang Di,
Lei Ling
Publication year - 2021
Publication title -
international journal of rheumatic diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 41
eISSN - 1756-185X
pISSN - 1756-1841
DOI - 10.1111/1756-185x.13962
Subject(s) - medicine , immunology , dermatomyositis , polymyositis , rheumatoid arthritis , pathogenesis , connective tissue , immune system , interleukin 17 , autoimmunity , pathology
Interleukin (IL)‐35 belongs to the IL‐12 cytokine family and is a heterodimer of the p35 and Epstein‐Barr virus‐induced gene 3 (EBI3) subunits. Functionally, IL‐35 can promote the proliferation and activation of regulatory T cells (Tregs) and suppress the function of T helper 17 (Th17) cells and other inflammatory cells to inhibit immune responses. In recent years, an abnormal IL‐35 expression causing a Th17/Treg imbalance has been associated with the development and progression of several connective tissue diseases (CTDs), such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), dermatomyositis (DM)/polymyositis (PM), and primary Sjögren’s syndrome (pSS). Here, we review the role of IL‐35 in regulating the balance of Th17/Treg responses in different types of CTDs and provide new insights into the role of IL‐35 in these diseases.