COMPLEMENT RECEPTOR IS AN INHIBITOR OF THE COMPLEMENT CASCADE
COMPLEMENT RECEPTOR IS AN INHIBITOR OF THE COMPLEMENT CASCADE
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DOI：
10.1084/jem.153.5.1138
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发表时间：
1981-01-01
影响因子：
15.3
通讯作者：
NUSSENZWEIG, V
中科院分区：
文献类型：
--
作者：
IIDA, K;NUSSENZWEIG, V
来自人红细胞膜的糖蛋白被鉴定为C3 B（补体成分3的B片段）（CR 1）的受体。它促进替代途径C3转化酶C3 b、Bb的解离以及C3 b/C4 b灭活剂对C3 b的切割。CR 1还使经典途径的C3和C5转化酶失活。CR 1抑制C3转化酶EAC 142（绵羊红细胞-抗体-补体复合物）对C3的消耗，并增强C4 b，2a位点的衰变。在重量基础上，CR 1比C4结合蛋白（C4 b，2a的血清抑制剂）的活性高5-10倍。C2抑制125 I-CR 1与EAC 14细胞的结合。CR 1和C2可能竞争C4 b上的位点。CR 1能更有效地抑制C5转化酶，但对晚期补体成分的组装没有影响。在高浓度下，单独的CR 1对细胞结合的C4 b没有不可逆的影响。在液相中，CR 1可以作为α-半乳糖苷酶裂解的辅因子。C3 b/C4 b失活剂对C4 b链的作用。CR 1的一个众所周知的功能是促进携带C3 b和C4 b的微生物或免疫复合物与细胞的粘附。这种相互作用可能导致对响应细胞的质膜的微环境损伤，因为外源性C3 b和C4 b片段可以充当级联的酶的组装的额外位点。细胞表面上的CR 1可以提供补体系统的扩增酶的强抑制剂的增加的局部浓度，并且可以为细胞提供当它们结合C3 b-和C4 b-承载底物时规避损伤的机制。
A glycoprotein from the membrane of human erythrocytes was identified as a receptor for C3b (b fragment of complement component 3) (CR1). It promotes the dissociation of the alternative pathway C3 convertase C3b,Bb and the cleavage of C3b by C3b/C4b inactivator. CR1 also inactivates the C3 and C5 convertases of the classical pathway. CR1 inhibits the consumption of C3 by C3 convertase EAC142 (sheep erythrocyte-antibody-complement complex) and enhances the decay of C4b,2a sites. On a weight basis, CR1 is 5-10 times more active than C4 binding protein, a serum inhibitor of C4b,2a. The binding of 125I-CR1 to EAC14 cells is inhibited by C2. CR1 and C2 probably compete for a site on C4b. CR1 inhibited C5 convertase even more effectively, but had no effect on the assembly of the late complement components. At high concentrations, CR1 alone has no irreversible effects on cell-bound C4b. In the fluid phase, CR1 can function as a cofactor for the cleavage of the .alpha.'' chain of C4b by C3b/C4b inactivator. A well-known function of CR1 is to promote adherence of microbes or immune complexes bearing C3b and C4b to cells. This interaction could result in a microenvironment damaging to the plasma membrane of the responding cell because the extrinsic C3b and C4b fragments can serve as additional sites of assembly of enzymes of the cascade. CR1 on the surface of cells may supply an increased local concentration of a strong inhibitor of the amplifying enzymes of the complement system and may provide cells with a mechanism for circumventing damage when they bind C3b- and C4b-bearing substrates.