Rheumatoid arthritis (RA) is one of the most common autoimmune diseases. Th17 has been shown to play am important role in the pathogenesis of RA. Accumulating data suggest the involvement of NLRP3 inflammasome in Th17 differentiation in autoimmune diseases. In the current study, we found that NLRP3 inflammasome is activated in CD4 T cells from RA patients. The activation of NLRP3 inflammasome was correlated with disease activities and IL-17A concentration in RA sera. Knockdown of NLRP3 suppressed Th17 differentiation. In addition, caspase-1 or IL-1 receptor inhibitor inhibits Th17 differentiation significantly. Further, ROS production is increased in CD4 T cells from RA patients. The inhibition of ROS production decreased NLRP3 inflammasome activation and IL-1β production in CD4 T cells, leading to the suppression of Th17 differentiation. These findings suggest a pathogenic role of NLRP3 inflammasome in RA by promoting Th17 cell differentiation. NLRP3 inflammasome could be a potential therapeutic target for the treatment of RA.

类风湿关节炎（RA）是最常见的自身免疫性疾病之一。Th17已显示在RA的发病机理中起重要作用。越来越多的数据表明，NLRP3炎性小体参与了自身免疫性疾病的Th17分化。在当前的研究中，我们发现NLRP3炎性小体在RA患者的CD4 T细胞中被激活。NLRP3炎性小体的激活与RA血清中的疾病活动和IL-17A浓度相关。敲低NLRP3抑制Th17分化。另外，caspase-1或IL-1受体抑制剂可显着抑制Th17分化。此外，来自RA患者的CD4T细胞中ROS产生增加。ROS产生的抑制作用会降低CD4 T细胞中NLRP3炎性体的激活和IL-1β的产生，从而抑制Th17分化。这些发现提示NLRP3炎性小体通过促进Th17细胞分化而在RA中具有致病作用。NLRP3炎性小体可能是治疗RA的潜在治疗靶标。