Role of anti-endothelial cell antibodies and transendothelial migratory T cells in the pathogenesis of autoimmune lesions

系统性红斑狼疮(SLE)患者血清中抗内皮细胞抗体水平升高，特别是那些有肺动脉高压、指状血管炎、雷诺现象或浆膜炎的患者。免疫印迹显示与抗内皮细胞抗体反应的抗原为36，37kD蛋白。对从人胎盘c DNA文库克隆的c DNA进行分析，证实核糖体P0蛋白为抗原。以重组融合蛋白为抗原，建立了抗核糖体P0蛋白抗体的酶联免疫吸附试验。抗核糖体P0抗体仅在SLE患者血清中呈阳性，且抗核糖体P0蛋白抗体阳性与狼疮精神病以外的中枢神经系统受累有关。类风湿关节炎的特征是慢性滑膜炎症，导致关节骨和软骨的破坏。表面表型为LFA-1(中等阳性)、CD26(高度阳性)的T细胞亚群的跨内皮细胞迁移参与了慢性滑膜炎的发病机制。在体外，这些T细胞亚群的抗原刺激激活可以被抗风湿药物如硫代马酸金钠、金诺芬或布比拉明所抑制。在对药物有反应的患者中观察到了更大的抑制水平，这表明这些评估可能具有预测价值。

Anti-endothelial cell antibody levels are elevated in sera from systemic lupus erythematosus (SLE) patients, especially in those who had pulmonary hypertension, digital vasculitis, Raynaud's phenomenon, or serositis. The antigens reacting with anti-endothelial cell antibodies is shown to be 36,37kD proteins by immunoblotting. The analysis of the cloned cDNA from human placenta cDNA library confirmed ribosomal P0 protein as the antigen. Enzyme-linked immunosorbent assay for anti-ribosomal P0 protein antibodies was established using recombinant fusion protein derived from cDNA as antigens. Anti-ribosomal P0 antibodies were positive only in sera from SLE patients, and positive anti-ribosomal P0 protein antibodies were correlated with central nervous system involvement other than lupus psychosis.Rheumatoid arthritis is characterized by chronic inflammation of synovium resulting in destruction of bone and cartilage of joints. Trans-endothelial migration of T cell subsets with surface phenotype of LFA-1 (intermediately positive), CD26 (highly positive) is involved in the pathogenesis of chronic synovitis. In vitro antigen-stimulated activation of those T cell subset is suppressed by disease-modifying anti-rheumatic drugs such as gold sodium thiomalate, auranofin or bucillamine. The greater level of suppression was observed in patients whoresponded the medication, indicating possible predicting value for these assessment