膝骨关节炎中天然免疫和TLR/NF-κB信号通路的研究进展

The research on natural immunity and Toll-like receptor/NF-κB signaling pathways in the knee osteoarthritis

膝骨关节炎(OA),是由多种因素引起关节软骨纤维化、破损、降解、脱失而导致的关节退行性疾病。目前,有越来越多的研究表明,骨关节炎的发生、进展有toll样受体(TLR)介导的天然免疫系统的参与,其中TLR/NF-κB信号通路扮演了重要角色。一般认为,遗传、代谢或机械因素造成关节软骨的初始伤害,导致软骨释放特定的自身抗原触发自身免疫反应。包括T细胞、B细胞和巨噬细胞在内的免疫细胞渗透到关节组织,释放各种细胞因子和趋化因子,例如基质金属蛋白酶(MMPs)和前列腺素E2(PGE2)释放,补体系统被激活,导致软骨降解,关节软骨进一步被破坏。本文回顾在OA发病机制中的天然免疫系统和TLR/NF-κB信号通路的作用。

Knee osteoarthritis is a degenerative joint disease induced by many factors and result in articular cartilage fibrosis, damage, degradation and depigmentation. Currently, there are an increasing number of studies have shown that Toll-like receptor （TLR） mediated innate immune system has participated in the incidence and progress of osteoarthritis, among which TLR/NF-κB signaling pathways play an important role. Genetic, metabolic or mechanical factors cause an initial injury to the cartilage resulting in release of several cartilage specific auto-antigens, which trigger the activation of immune response. Immune cells including T cells, B cells and macrophages infiltrate the joint tissues, cytokines and chemokines are released from different kinds of cells present in the joint, complement system is activated, and cartilage degrading factors such as matrix metalloproteinases （MMPs） and prostaglandin E2 （PGE2） are released, resulting in further damage to the articular cartilage.Here we reviewed the studies implicating nature immune system and the TLR/NF-κB signaling pathways in the pathogenesis of osteoarthritis.