Abstract：
Osteoarthritis (OA) is one of the most common degenerative diseases characterised by joint pain, swelling and decreased mobility, with its main pathological features being articular synovitis, cartilage degeneration and osteophyte formation. Inflammatory cytokines and chemokines secreted by activated immunocytes can trigger various inflammatory and immune responses in articular cartilage and synovium, contributing to the genesis and development of OA. A series of monocyte/macrophage chemokines, including monocyte chemotaxis protein (MCP)-1/CCL2, MCP2/CCL8, macrophage inflammatory protein (MIP)-1α/CCL3, MIP-1β/CCL4, MIP-3α/CCL20, regulated upon activation, normal T-cell expressed and secreted /CCL5, CCL17 and macrophage-derived chemokine/CCL22, was proven to transmit cell signals by binding to G protein-coupled receptors on recipient cell surface, mediating and promoting inflammation in OA joints. However, the underlying mechanism of these chemokines in the pathogenesis of OA remains still elusive. Here, published literature was reviewed, and the function and mechanisms of monocyte/macrophage chemokines in OA pathogenesis were summarised. The symptoms and disease progression of OA were found to be effectively alleviated when the expression of these chemokines is inhibited. Elucidating these mechanisms could contribute to further understand how OA develops and provide potential targets for the early diagnosis of arthritis and drug treatment to delay or even halt OA progression.
摘要：
骨关节炎（OA）是以关节疼痛为特征的最常见的退行性疾病之一，肿胀和流动性下降，其主要病理特征是关节滑膜炎，软骨退化和骨赘形成。活化的免疫细胞分泌的炎性细胞因子和趋化因子可在关节软骨和滑膜中引发各种炎症和免疫反应。有助于OA的发生和发展。一系列单核细胞/巨噬细胞趋化因子，包括单核细胞趋化蛋白（MCP）-1/CCL2，MCP2/CCL8，巨噬细胞炎性蛋白（MIP）-1α/CCL3，MIP-1β/CCL4，MIP-3α/CCL20，在激活时调节，正常T细胞表达和分泌/CCL5，CCL17和巨噬细胞衍生的趋化因子/CCL22被证明通过与受体细胞表面的G蛋白偶联受体结合来传递细胞信号，介导和促进OA关节的炎症。然而,这些趋化因子在OA发病中的潜在机制仍然难以捉摸。这里,发表的文献进行了回顾，并对单核细胞/巨噬细胞趋化因子在OA发病中的作用及机制进行了综述。发现当这些趋化因子的表达被抑制时,OA的症状和疾病进展被有效地减轻。阐明这些机制可能有助于进一步了解OA是如何发展的，并为关节炎的早期诊断和药物治疗提供潜在的靶标，以延迟甚至停止OA的进展。
