Author:
Han Liang,Chen Zhe,Yu Kun,Yan Jiahui,Li Tingting,Ba Xin,Lin Weiji,Huang Yao,Shen Pan,Huang Ying,Qin Kai,Geng Yinhong,Liu Yafei,Wang Yu,Tu Shenghao
Abstract
The occurrence and development of rheumatoid arthritis (RA) is regulated by numerous cytokines. Interleukin 27 (IL-27) is a soluble cytokine that exerts biological effects by regulating the Janus tyrosine kinase (JAK)/signal transducer and activator of the transcription (STAT) signaling pathwayviathe IL-27 receptor. IL-27 is known for its pleiotropic roles in modulating inflammatory responses. Previous studies found that IL-27 levels are elevated in RA blood, synovial fluid, and rheumatoid nodules. Cellular and animal experiments indicated that IL-27 exerts multiple regulatory functions in RA patientsviadifferent mechanisms. IL-27 inhibits ectopic-like structure (ELS) formation and CD4+T helper type 2 (Th2) cell, CD4+T helper type 17 (Th17) cell, and osteoclast differentiation in RA, contributing to alleviating RA. However, IL-27 promotes Th1 cell differentiation, which may exacerbate RA synovitis. Moreover, IL-27 also acts on RA synovial fibroblasts (RA-FLSs) and regulatory T cells (Tregs), but some of its functions are unclear. There is currently insufficient evidence to determine whether IL-27 promotes or relieves RA. Targeting IL-27 signaling in RA treatment should be deliberate based on current knowledge.
Funder
National Natural Science Foundation of China
Subject
Immunology,Immunology and Allergy
Cited by
8 articles.
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