类风湿关节炎（rheumatoid arthritis，RA）是一种慢性进行性的自身免疫病，其发病机制尚未明确。在RA发生与发展过程中，细胞因子起到了重要作用。近年来针对细胞因子参与自身免疫病的研究发现，作为白细胞介素-1（interleukin-1，IL-1）家族的新成员，IL-37能够通过胞外与膜受体结合、胞内形成复合物2种方式参与调控信号通路，发挥其抗炎作用。研究表明，IL-37在健康人群体内的表达水平极低，在RA患者体内则过表达；且在RA患者血清中，IL-37水平与肿瘤坏死因子α、IL-6、IL-1α等促炎因子水平，C反应蛋白水平以及疾病活动分数28评分等呈正相关。然而，给予IL-37可以缓解胶原诱导的关节炎小鼠的炎症及病理症状，继而表明IL-37可能以负反馈的方式在RA中起着抑制炎症的作用，具体抗炎机制可能与SMAD家族成员3、核因子κB等信号通路有关。该文就IL-37的结构与表达、受体及其信号通路、功能及其在RA中的作用机制进行综述，为IL-37及RA的后续研究提供思路与参考。

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.