Ospelt Caroline, Gay Steffen
Center of Experimental Rheumatology, University Hospital Zurich and Zurich Center of Integrative Human Physiology, Gloriastrasse 23, CH-8091 Zürich, Switzerland.
Best Pract Res Clin Rheumatol. 2008 Apr;22(2):239-52. doi: 10.1016/j.berh.2008.01.004.
Infiltration by inflammatory cells, thickening of the lining layer, and destructive invasion into cartilage and bone are pathognomic features of the synovium in rheumatoid arthritis (RA). However, the most common cell types at the sites of invasion are resident cells of the joint, in particular synovial fibroblasts. These cells differ from healthy synovial fibroblasts in their morphology, their expression of proto-oncogenes and antiapoptotic molecules, and in their lack of certain tumor suppressor genes. Through their production of proinflammatory cytokines and chemokines mediated by signaling via Toll-like receptors, they are not only effector cells but also active parts of the innate immune system attracting inflammatory immune cells to the synovium. Most importantly, by producing matrix-degrading molecules they contribute strongly to the destructive mechanisms operative in RA.
炎症细胞浸润、衬里层增厚以及对软骨和骨的破坏性侵袭是类风湿关节炎（RA）滑膜的特征性表现。然而，侵袭部位最常见的细胞类型是关节的常驻细胞，尤其是滑膜成纤维细胞。这些细胞在形态、原癌基因和抗凋亡分子的表达以及某些肿瘤抑制基因的缺失方面与健康滑膜成纤维细胞不同。通过Toll样受体介导的信号传导产生促炎细胞因子和趋化因子，它们不仅是效应细胞，也是先天性免疫系统的活跃部分，可将炎症免疫细胞吸引至滑膜。最重要的是，通过产生基质降解分子，它们对RA中的破坏机制有很大贡献。
