Lysis of erythrocytes by complement in the absence of antibody.
Lysis of erythrocytes by complement in the absence of antibody.
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DOI：
10.1084/jem.132.5.898
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发表时间：
1970-11
期刊：
影响因子：
--
通讯作者：
Müller-Eberhard HJ
中科院分区：
文献类型：
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作者：
Götze O;Müller-Eberhard HJ
一种新的补体介导的溶血途径已被描述。它不依赖于抗体，不需要前四种补体成分与靶细胞表面结合。对靶细胞的实际攻击开始于C5、C6和C7的附着。结合反应由C4，2，3催化，C4，2，3是一种可以在无细胞溶液中形成的酶。C4、2、3可通过从流体相或从其特异性结合的另一个细胞的表面起作用来影响C5、6、7的结合（EAC 4、2、3）。在任一种情况下，所得产物为EC 5、6、7，其对C8和C9的裂解敏感。来自阵发性睡眠性血红蛋白尿症（PNH）患者的红细胞特别易受上述机制的溶解。PNH细胞，而不是正常的人红细胞，也可以通过激活补体的眼镜蛇因子裂解。这些观察允许补体的激活和攻击机制的操作区别。
A new pathway of complement-mediated hemolysis has been described. It is independent of antibody and does not require binding of the first four complement components to the target-cell surface. The actual attack of the target cell begins with the attachment of C5, C6, and C7. The binding reaction is catalyzed by C4, 2, 3, an enzyme which may be formed in cell-free solution. C4, 2, 3 may effect binding of C5, 6, 7 by acting from the fluid phase or from the surface of another cell to which it is specifically bound (EAC 4, 2, 3). In either case, the resulting product is EC5, 6, 7 which is susceptible to lysis by C8 and C9. Erythrocytes from patients with paroxysmal nocturnal hemoglobinuria (PNH) were particularly susceptible to lysis by the above described mechanism. PNH cells, but not normal human erythrocytes, could also be lysed through activation of complement by cobra factor. These observations allow the operational distinction of an activation and an attack mechanism of complement.