Rheumatoid arthritis (RA) is an autoimmune inflammatory disease characterized by the destruction of cartilage and bone. The present study aims to investigate the role of HtrA serine peptidase 2 (HtrA2) in the collagen-induced arthritis. The expressions of HtrA2 were determined in the database BioGPS and bone marrow-derived macrophages (BMDMs). The populations of myeloid and lymphoid cells were determined in wild type and HtrA2 knockout (HtrA2^MKO) mice using flow cytometry. In addition, the expressions of pro-inflammatory cytokines (Il6, Tnf, and Il1β) were determined in the activated BMDMs from wild type (WT) and HtrA2^MKO mice. STRING database was used to predict the interactive proteins of HtrA2 and Co-Immunoprecipitation was used to confirm these interactions. A collagen-induced arthritis model was established to investigate the effects of HtrA2 on the arthritis symptoms. It was found that HtrA2 reduction was associated with the activation of myeloid cells. Interestingly, HtrA2 deficiency did not affect the development of myeloid and lymphoid cells. Further studies demonstrated that HtrA2 deficiency suppressed the production of pro-inflammatory cytokines in BMDMs induced by lipopolysaccharide or CpG. Co-Immunoprecipitation results demonstrated that HtrA2 enhanced the stability of TNF receptor-associated factor 2 (TRAF2). HtrA2 participated in the activation of the inflammatory response in a collagen-induced arthritis model. In summary, HtrA2 modulates inflammatory responses in BMDMs by controlling TRAF2 stability in a collagen-induced arthritis mouse model.

类风湿关节炎（RA）是一种自身免疫性炎性疾病，其特征在于软骨和骨骼的破坏。本研究旨在调查HtrA丝氨酸肽酶2（HtrA2）在胶原诱导的关节炎中的作用。HtrA2的表达是在BioGPS和骨髓巨噬细胞（BMDMs）数据库中确定的。使用流式细胞仪确定野生型和HtrA2基因敲除（HtrA2 ^MKO）小鼠中的髓样和淋巴样细胞的群体。此外，确定了野生型（WT）和HtrA2 ^MKO激活的BMDM中促炎细胞因子（Il6，Tnf和Il1β）的表达。老鼠。使用STRING数据库预测HtrA2的相互作用蛋白，并使用共免疫沉淀法确认这些相互作用。建立胶原诱导的关节炎模型以研究HtrA2对关节炎症状的影响。发现HtrA2的减少与髓样细胞的活化有关。有趣的是，HtrA2缺乏症并不影响髓样和淋巴样细胞的发育。进一步的研究表明，HtrA2缺乏抑制了脂多糖或CpG诱导的BMDM中促炎性细胞因子的产生。免疫共沉淀结果表明，HtrA2增强了TNF受体相关因子2（TRAF2）的稳定性。HtrA2参与了胶原诱导的关节炎模型中炎症反应的激活。综上所述，