CAJ | 학술논문

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。
슬골관절염（OA），시유다충인소인기관절연골섬유화、파손、강해、탈실이도치적관절퇴행성질병。목전，유월래월다적연구표명，골관절염적발생、진전유toll양수체（TLR）개도적천연면역계통적삼여，기중TLR/NF-κB신호통로분연료중요각색。일반인위，유전、대사혹궤계인소조성관절연골적초시상해，도치연골석방특정적자신항원촉발자신면역반응。포괄T세포、B세포화거서세포재내적면역세포삼투도관절조직，석방각충세포인자화추화인자，례여기질금속단백매（MMPs）화전렬선소 E2（PGE2）석방，보체계통피격활，도치연골강해，관절연골진일보피파배。본문회고재 OA 발병궤제중적천연면역계통화TLR/NF-κB신호통로적작용。
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.