辅助性T细胞在痛风发病机制中的研究进展

Research Progress of Helper T Cell in Pathogenesis of Gout

痛风是由单钠尿酸盐(MSU)晶体沉积于关节组织引起的自身炎症性疾病,也是最常见的炎症性关节炎。痛风的病理过程涉及固有免疫反应和适应性免疫反应。巨噬细胞和中性粒细胞是参与痛风发病的主要免疫细胞,MSU晶体介导的核苷酸结合寡聚化结构域样受体蛋白3炎症小体和Toll样受体激活是痛风炎症的关键机制。CD4^(+)T细胞也参与痛风的免疫发病机制,辅助性T细胞(Th细胞)功能异常、Th细胞活化所需的转录因子异常以及其分泌的标志性细胞因子表达异常均可能是导致痛风发生的主要原因。因此,深入研究痛风的发病机制,可以为疾病的治疗提供新思路。

Gout is an autoinflammatory disease caused by the deposition of monosodium urate(MSU)crystals in joint tissues and is the most common form of inflammatory arthritis.The pathological process of gout involves both innate and adaptive immune responses.Macrophages and neutrogranulocytes are the main immune cells involved in the pathogenesis of gout.MSU crystal-mediated nucleotide-binding oligomerized domain-like receptor protein 3 inflammasomes and Toll-like receptor activation are the key mechanisms of gout inflammation.CD4^(+)T cell is also involved in the immune pathogenesis of gout.Abnormal function of helper T cell(Th cell),abnormal transcription factors required for Th cell activation,and abnormal expression of signature cytokines secreted by them may be the main causes of gout.Therefore,in-depth study of the pathogenesis of gout can provide new ideas for the treatment of the disease.