Production of ultrastructural membrane lesions by the fifth component of complement.

Production of ultrastructural membrane lesions by the fifth component of complement.
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DOI:
10.1084/jem.133.1.53
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发表时间:
1971-01-01
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
Feldman JD
Feldman JD
中科院分区:
其他
文献类型:
--
作者:
Polley MJ;Müller-Eberhard HJ;Feldman JD

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已证明细胞结合的 C4,2 复合物或 C5 分子的数量与免疫溶血后细胞膜上可见的超微结构损伤的数量之间存在直接的定量关系。当结合的C4,2复合物超过结合的C5分子时,所看到的超微结构损伤的数量与C5分子的数量相对应。然而,在相反的情况下,结合的 C5 分子超过结合的 C4,2 复合物,后者决定了病变的数量。在补体反应序列中,损伤首先在非裂解中间复合物 EAC1,4,2,3,5 中变得可见,并且当 C6-C9 诱导裂解时,其数量不受影响。由于中间复合体 EC5、6、7 上也出现了损伤,因此可以得出结论,蛋白质 C5 负责其产生。一旦形成,病变的表现就不再需要 C5 分子的物理存在,如胰蛋白酶去除 C5 蛋白后病变的持续存在所表明的。因此,C5 依赖性超微结构现象被解释为代表膜的真实结构变化,然而,该变化并不伴随渗透性缺陷。
A direct quantitative relationship has been demonstrated between the number of cell bound C4,2 complexes or C5 molecules and the number of ultrastructural lesions visualized on the cell membrane subsequent to immune hemolysis. When bound C4,2 complexes exceeded bound C5 molecules, the number of ultrastructural lesions seen corresponded to the number of C5 molecules. However, in the reverse situation, with bound C5 molecules in excess of bound C4,2 complexes, the latter determined the number of lesions. During the complement-reaction sequence, the lesions first became visible in the nonlytic intermediate complex EAC1,4,2,3,5 and their number was unaffected when lysis was induced by C6–C9. Since the lesions were also demonstrable on the intermediate complex EC5,6,7, it is concluded that the protein C5 is responsible for their production. Once formed, the physical presence of the C5 molecule is no longer required for the manifestation of the lesions as indicated by persistence of lesions after removal of C5 protein by trypsin. The C5-dependent ultra-structural phenomenon has therefore been interpreted to represent a true structural change of the membrane which, however, is not accompanied by a permeability defect.
正常人和阵发性夜间血红蛋白尿(PNH)红细胞的免疫裂解。 3。由补体裂解引起的膜缺陷。
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