Veterans Affairs Medical Center and University of California San Diego, 3350 La Jolla Village Drive, 111K, San Diego, CA 92161, USA.
Curr Rheumatol Rep. 2013 May;15(5):323. doi: 10.1007/s11926-013-0323-5.
This review focuses on the recent advancements in the understanding of innate immunity in the pathogenesis of osteoarthritis, particularly with attention to the roles of damage-associated molecular patterns (DAMPs), pattern recognition receptors (PPRs), and complement in synovitis development and cartilage degradation. Endogenous molecular products derived from cellular stress and extracellular matrix disruption can function as DAMPs to induce inflammatory responses and pro-catabolic events in vitro and promote synovitis and cartilage degradation in vivo via PRRs. Some of the DAMPs and PRRs display various capacities in driving synovitis and/or cartilage degradation in different models of animal studies. New findings reveal that the inflammatory complement cascade plays a key in the pathogenesis of OA. Crosstalk between joint tissues such as synovium and cartilage communicated at the cellular level within the innate immune inflammatory network is implicated to play an important role in OA progression. Further studies on how the innate immune inflammatory network impacts the OA disease process at different stages of progression will lead to the development of new therapeutic strategies.
本篇综述聚焦于固有免疫在骨关节炎发病机制中的最新研究进展，特别关注损伤相关分子模式（DAMPs）、模式识别受体（PPRs）和补体在滑膜炎发展和软骨降解中的作用。源自细胞应激和细胞外基质破坏的内源性分子产物可作为 DAMPs，通过 PPRs 在体外诱导炎症反应和促分解代谢事件，并在体内促进滑膜炎和软骨降解。一些 DAMPs 和 PPRs 在不同的动物模型中显示出不同的驱动滑膜炎和/或软骨降解的能力。新的研究发现，炎症补体级联反应在 OA 的发病机制中起着关键作用。关节组织（如滑膜和软骨）之间的细胞水平上的相互作用，在固有免疫炎症网络中，被认为在 OA 的进展中起着重要作用。进一步研究固有免疫炎症网络如何在 OA 进展的不同阶段影响疾病过程，将导致新的治疗策略的发展。
