Kawaguchi T, Nakakuma H
Second Department of Internal Medicine, Kumamoto University School of Medicine.
Nihon Rinsho. 1996 Sep;54(9):2370-5.
Decay-accelerating factor (DAF) and CD59 are major complement regulators linked to plasma membrane via glycosylphosphatidylinositol anchor and inhibit C3 activation and the formation of membrane attack complex, respectively. These factors have been shown to protect human erythrocytes from the lytic action of autologous complement. Here we overview structure and function of these molecules, and discuss about their physiological roles in controlling the complement activation, ie, defining the susceptibility of erythrocytes to complement.
衰变加速因子(DAF)和CD59是通过糖基磷脂酰肌醇锚定连接到质膜的主要补体调节因子,分别抑制C3活化和膜攻击复合物的形成。这些因子已被证明可保护人类红细胞免受自身补体的溶解作用。在此,我们概述这些分子的结构和功能,并讨论它们在控制补体激活中的生理作用,即确定红细胞对补体的易感性。