Liao H X, Haynes B F
Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA.
Rheum Dis Clin North Am. 1995 Aug;21(3):715-40.
The pathogenesis of rheumatoid arthritis centers on as yet unknown initiating events in the synovium that result in synovial vessel proliferation, and upregulation of endothelial cell ligands for leukocyte adhesion molecules. Ligation of adhesion molecules on synovial microenvironment cells and immune cells probably regulates synovial and immune cell inflammatory cytokine production. Interruption of adhesion molecule function and interruption of inflammatory cytokine production are promising new sites of therapeutic inhibition of synovial inflammation.
类风湿性关节炎的发病机制集中于滑膜中尚不明确的起始事件,这些事件导致滑膜血管增生以及白细胞粘附分子的内皮细胞配体上调。滑膜微环境细胞和免疫细胞上粘附分子的结合可能调节滑膜和免疫细胞炎性细胞因子的产生。粘附分子功能的阻断以及炎性细胞因子产生的阻断是滑膜炎症治疗性抑制的有前景的新靶点。