巨噬细胞及其表达和分泌产物在类风湿性关节炎发病中的作用

巨噬细胞分化自外周血单核细胞，二者在类风湿性关节炎（rheumatoid arthritis, RA）的发病过程中起着关键性的作用。这些细胞参与了炎症的启动和维持、白细胞的黏附和迁移、基质的降解和血管新生。巨噬细胞表达黏附分子、趋化因子受体（chemokine receptor，CR）和其他表面抗原；它们还分泌趋化因子、细胞因子、生长因子、蛋白酶和其他介质。这些炎症介质是关节炎中炎症和血管新生发生的重要病理机制。近年来，巨噬细胞移动抑制因子（macrophage migration inhibitory factor, MIF）受到研究者们的广泛关注，这种细胞因子可由包括巨噬细胞在内的多种细胞产生，它反过来可以促进巨噬细胞的活化和细胞因子的产生；同时，它可以调节机体对糖皮质激素的敏感性；并且将类风湿性关节炎与动脉粥样硬化等炎症疾病联系在一起。在类风湿性关节炎发病过程中，巨噬细胞还可以产生多种蛋白酶（如组织蛋白酶G，cathepsin G），这些蛋白酶促进了炎症和血管新生的发生。鉴于巨噬细胞及其表达和分泌产物在类风湿关节炎致病机理中具有关键性作用，它们已成为治疗类风湿性关节炎的一个理想靶点。

Role of Macrophages and Their Products in the Pathogenesis of Rheumatoid Arthritis

Abstract〖WTB1]Macrophages differentiate from peripheral blood monocytes. Both monocytes and synovial macrophages are key players in rheumatoid arthritis. These cells are involved in the initiation and perpetuation of inflammation, leukocyte adhesion and migration, matrix degradation and angiogenesis. Macrophages express adhesion molecules, chemokine receptors and other surface antigens. They also secrete a number of chemokines, cytokines, growth factors, proteases and other mediators. These inflammatory mediators are the pathological mechanisms of inflammation and angiogenesis in arthritis. In recent years, macrophage migration inhibitory factor has drawn great attention. This cytokine is involved in macrophage activation and cytokine production. Meanwile, migration inhibitory factor also regulates glucocorticoid sensitivity and may be a pathogenic link between rheumatoid arthritis and atherosclerosis. In rheumatoid arthritis, several proteinases including cathepsin G are produced by macrophages, and they are associated with inflammatory and angiogenic events. As macrophages and their products are key players in the pathogenesis of rheumatoid arthritis, they may become good therapeutic targets for treating arthritis.