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膜联蛋白A2(AXⅡ)在自身免疫性疾病中往往高表达,并可作为自身抗体——抗AXⅡ抗体的靶点而起作用。在抗磷脂抗体综合症中,内皮细胞上的β2糖蛋白-1结合AXⅡ,利用Toll样受体-4作为共受体,通过特异性结合抗磷脂抗体/抗β2糖蛋白-1抗体触发细胞内信号通路,从而诱导炎性反应或血栓形成。狼疮性肾炎的抗ds-DNA抗体依赖AXⅡ结合肾小球系膜细胞后,进入细胞质和细胞核,激活p38 MAPK、JNK、AKT通路,诱导IL-6分泌和AXⅡ合成,形成恶性循环而不断加剧肾炎进展。类风湿关节炎患者滑膜组织中的AXⅡ高表达,a AXⅡ呈高水平。可见,AXⅡ通过不同的途径参与了自身免疫性疾病的多个致病环节:1)与自身抗体的抗原相互结合,并且促进炎性细胞因子表达及病理变化;2)直接与自身抗体结合,介导信号通路的激活,从而诱导炎症因子的分泌。
Annexin A2 (AXII) is often overexpressed in autoimmune diseases and can function as a target of autoantibody-anti-AXII antibodies. In the antiphospholipid antibody syndrome, β2 glycoprotein-1 binds to AXII on endothelial cells, uses Toll-like receptor-4 as a co-receptor and triggers intracellular by specific binding of antiphospholipid antibody / anti-β2 glycoprotein-1 antibody Signaling pathways to induce inflammatory responses or thrombosis. Anti-ds-DNA antibody of lupus nephritis relies on AXⅡ to bind to mesangial cells and then enter the cytoplasm and nucleus, activating p38 MAPK, JNK and AKT pathways, inducing IL-6 secretion and AXⅡ synthesis, forming a vicious circle and aggravating nephritis progress. In rheumatoid arthritis patients, the expression of AX Ⅱ in synovium was high, a AX Ⅱ was high. It can be seen that AXII participates in multiple pathogenic stages of autoimmune diseases through different pathways: 1) binding to antigens of autoantibodies and promoting the expression of inflammatory cytokines and pathological changes; 2) directly binding to autoantibodies, Activation of signaling pathways, thereby inducing the secretion of inflammatory cytokines.