Müller-Ladner U
Department of Medicine, University of Alabama at Birmingham 35294-0006, USA.
Curr Opin Rheumatol. 1995 May;7(3):222-8. doi: 10.1097/00002281-199505000-00011.
An appreciation of the role of T cell-independent pathways in the pathogenesis of rheumatoid arthritis (RA) has led to significant advances. New approaches have included the identification of novel cytokines and growth factors and characterization of the recently defined chemokines. Greater insight has been achieved with regard to prostaglandin pathways and the role of the synovial matrix and vasculature. The synovial matrix contributes to cell regulation in RA to a greater extent than previously believed, and the vasculature of the synovium must now be regarded as an active participant in the regulation of cell growth. The most exciting development, however, is the recognition of the involvement of oncogenes and apoptosis pathways in the dysregulation of the synovial cell cycle, which presumably causes the continuous synovial growth that is characteristic of RA.
对类风湿性关节炎（RA）发病机制中T细胞非依赖途径作用的认识取得了重大进展。新方法包括鉴定新型细胞因子和生长因子以及对最近定义的趋化因子进行表征。在前列腺素途径以及滑膜基质和脉管系统的作用方面有了更深入的了解。滑膜基质对RA中细胞调节的作用比以前认为的更大，现在必须将滑膜脉管系统视为细胞生长调节的积极参与者。然而，最令人兴奋的进展是认识到癌基因和细胞凋亡途径参与滑膜细胞周期失调，这可能导致RA特有的滑膜持续生长。
