Daha M R
Department of Nephrology, University Hospital Leiden, The Netherlands.
Behring Inst Mitt. 1993 Aug(92):184-90.
Potentially, damage to endothelial cells of small vessel walls may be induced by the deposition of immune complexes and subsequent complement activation. The degree of deposition of C3b onto the endothelial cell surface under normal conditions is regulated by a number of membrane-bound regulators. Under inflammatory conditions various cytokines could potentially deregulate the expression and function of the membrane-bound complement inhibitors. Such a process could potentially increase the susceptibility of the endothelial cell layer to complement-mediated attack and provoke a vascular lesion.
潜在地,免疫复合物的沉积及随后的补体激活可能会诱导小血管壁内皮细胞的损伤。正常情况下,C3b在内皮细胞表面的沉积程度受多种膜结合调节因子的调控。在炎症条件下,各种细胞因子可能会解除对膜结合补体抑制剂表达和功能的调控。这样一个过程可能会增加内皮细胞层对补体介导攻击的易感性,并引发血管病变。