Review

Research progress of mechanism of IL-37 in rheumatoid arthritis

  • HUANG Run-qi ,
  • WANG An-ni ,
  • CHEN Guang-jie
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  • Department of Immunology and Microbiology, Shanghai Jiao Tong University College of Basic Medical Sciences, Shanghai 200025, China

Online published: 2020-04-09

Supported by

2017 RBL Project of Shanghai Jiao Tong University School of Medicine; National Natural Science Foundation of China (81771731).

Abstract

Rheumatoid arthritis (RA) is a chronic progressive autoimmune disorder, the mechanism of which is not clear yet. Cytokines play a key role in the pathogenesis of RA. Recent studies on cytokine involvement in autoimmune diseases have found that, as a new member of interleukin-1 (IL-1) family, IL-37 can participate in the regulation of signaling pathway and play its anti-inflammatory roleextracellular binding to membrane receptor and intracellular complex formation. Studies have shown that the level of IL-37 in healthy people is extremely low and overexpressed in RA patients, and the serum level of IL-37 in RA patients is positively correlated with the level of pro-inflammation cytokines such as tumor necrosis factor-α (TNF-α), IL-6 and IL-1α, the level of C reactive protein and 28-joint disease activity score (DAS28). However, IL-37 treatment can alleviate the inflammation and pathological symptoms of collagen-induced arthritis (CIA) mice, which indicates that IL-37 has anti-inflammatory effect via negative feedback. The specific anti-inflammatory mechanism may be related to mothers against decapentaplegic homolog 3 (SMAD3) pathway and nuclear factor kappa-B (NF-κB) pathway. This article reviews the structure and of IL-37, the receptor and its signal pathway and the function and its mechanism in RA, which provides references for the further study of IL-37 and RA.

Cite this article

HUANG Run-qi , WANG An-ni , CHEN Guang-jie . Research progress of mechanism of IL-37 in rheumatoid arthritis[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2020 , 40(3) : 391 . DOI: 10.3969/j.issn.1674-8115.2020.03.019

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