固有免疫系统在骨关节炎发病机制中的作用及研究进展

Role and progress of innate immunity in pathogenesis of osteoarthritis

目的综述固有免疫系统在骨关节炎(osteoarthritis,OA)发病机制中的作用及研究进展。方法查阅国内外相关文献,对固有免疫系统介导的炎症及巨噬细胞、T细胞、补体系统在OA发病机制中的作用、潜在治疗靶点及研究进展进行总结。结果随着研究深入,OA逐渐被认为是一种低度炎症状态,固有免疫系统在其发生发展过程中发挥了重要作用。目前研究主要集中于OA滑膜组织巨噬细胞亚群极化方面,结果显示M1亚群向M2亚群转换失败是OA进展的关键环节。而T细胞及补体系统也参与了OA的病理过程。结论目前有关固有免疫系统对OA进展作用的研究仍处于探索阶段,具体机制尚未明确。现有研究结果提示,巨噬细胞亚群极化是早期防治OA的潜在靶点。

Objective To review and summarize the role and progress of innate immunity in the pathogenesis of osteoarthritis(OA). Methods The domestic and foreign literature in recent years was reviewed. The role of innate immune-mediated inflammation, macrophages, T cells, and complement systems in the pathogenesis of OA, potential therapeutic targets, and the latest research progress were summarized. Results With the deepening of research, OA is gradually considered as a low-grade inflammation, in which innate immunity plays an important role. The polarization of synovial macrophage subpopulation in OA has been studied extensively. Current data shows that the failure of transformation from M1 subtype to M2 subtype is a key link in the progression of OA. T cells and complement system are also involved in the pathological process of OA. Conclusion At present, the role of innate immunity in the progress of OA has been played in the spotlight, whereas the specific mechanism has not been clear. The macrophage subtype polarization is a potential therapeutic target for early prevention and treatment of OA.