Schifferli J A, Steiger G, Schapira M
Clin Exp Immunol. 1985 Jun;60(3):605-12.
To clarify the mechanism of inhibition of immune precipitation by early components of the classical pathway of complement, aggregation of 125I-BSA-rabbit-anti-BSA antibody complexes was performed in the presence of purified C1, C1-inactivator (C1-In) and C4. C1 delayed the rate of immune precipitation in a concentration dependent manner. This phenomenon was not influenced by the presence of 0.3 mM p-nitrophenyl-p-guanidinobenzoate (NPGB) which inhibits C1 activation. The antiaggregational effect of C1 was reversed by 10 mM EDTA and by C1-In at a C1-In/C1 molar ratio of greater than or equal to 4/1. C1-In was not effective when the reaction was performed in the presence of NPGB. Thus, although the inhibitory effect of C1 on immune precipitation was not dependent upon C1 activation, the formation of C1 was required to observe the effect of C1-In. The addition of C4 to C1 did not modify the slow aggregation of complexes, even when a limiting concentration of C1 was used. C1-In and EDTA were both able to cause similar rapid precipitation of complexes prepared in the presence of C1 and C4, demonstrating that C4 did not play a significant role in delaying the precipitation reaction. However, soluble complexes prepared in the presence of C1 and C4 were specifically precipitated by the addition of excess anti-C4 antibody, attesting to the binding of C4 to immune complexes. These observations suggest that the processing of immune complexes in vivo may not be similar in different classical pathway complement deficiency states.
为阐明补体经典途径早期成分抑制免疫沉淀的机制，在纯化的C1、C1灭活剂（C1-In）和C4存在的情况下进行了125I-牛血清白蛋白-兔抗牛血清白蛋白抗体复合物的聚集实验。C1以浓度依赖的方式延缓了免疫沉淀的速率。这种现象不受抑制C1激活的0.3 mM对硝基苯基-对胍基苯甲酸（NPGB）存在的影响。C1的抗聚集作用可被10 mM乙二胺四乙酸（EDTA）以及C1-In/C1摩尔比大于或等于4/1的C1-In逆转。当反应在NPGB存在的情况下进行时，C1-In无效。因此，尽管C1对免疫沉淀的抑制作用不依赖于C1的激活，但观察C1-In的作用需要C1的形成。即使使用限量浓度的C1，向C1中添加C4也不会改变复合物的缓慢聚集。C1-In和EDTA都能够使在C1和C4存在下制备的复合物发生类似的快速沉淀，这表明C4在延缓沉淀反应中没有发挥重要作用。然而，在C1和C4存在下制备的可溶性复合物通过添加过量的抗C4抗体而被特异性沉淀，证明C4与免疫复合物结合。这些观察结果表明，在不同的经典途径补体缺陷状态下，体内免疫复合物的处理可能并不相同。
