Toll样受体7介导免疫炎症与类风湿关节炎的发病机制

Toll-like receptor 7 in immune inflammation and the pathogenesis of rheumatoid arthritis

Toll样受体(TLRs)是一种模式识别受体,表达于多种不同类型的细胞,其在炎症反应、细胞信号转导和免疫监视中均起重要作用。TLRs通过识别各自不同的配体,触发髓样细胞分化因子88(MyD88)依赖性和非依赖性通路,导致促炎性细胞因子和共刺激分子的激活,从而诱发局部炎症反应。而自身免疫性疾病的发生与免疫细胞及免疫因子异常相关。有研究表明,TLR7参与了类风湿关节炎的发生、发展。本文对TLR7及其参与类风湿关节炎发病机制的研究进展进行综述,旨在为该疾病的诊疗提供新的思路与理论依据。

Toll-like receptor(TLRs) is a pattern recognition receptor expressed in many different types of cells.It plays an important role in cellular inflammatory response,signal transduction and immune surveillance.By recognizing a large variety of ligands,TLRs triggers myeloid differentiation factor 88(MyD88)-dependent and independent pathways of myeloid cells,leading to the activation of pro-inflammatory cytokines and costimulatory molecules,thus inducing local inflammatory response.The occurrence of autoimmune diseases is related to the abnormality of immune cells and their factors.Several studies have determined that TLR7 is involved in the occurrence and development of rheumatoid arthritis(RA).This article reviews the research progress of TLR7 and its involvement in RA pathogenesis to provide new ideas and theoretical basis for the diagnosis and treatment of the disease.