Schifferli J A, Woo P, Peters D K
Clin Exp Immunol. 1982 Mar;47(3):555-62.
This study has examined the mechanisms involved in complement-mediated inhibition of immune precipitation using radiolabelled BSA and rabbit anti-BSA. Purified proenzyme C1 was capable of maintaining the complexes in soluble form during the first few minutes of reaction whereas immune precipitation was immediate in the presence of purified C1q or C1 + EDTA (ethylenediamine tetra-acetate). In C1q deficient serum, initial immune aggregation was followed by partial solubilization of the formed precipitate similar to that obtained with normal human serum in the presence of Mg EGTA. In C2 deficient serum precipitation occurred at a slow rate. Repletion of the deficient component (C1q or C2 respectively) restored fully inhibition of precipitation. These experiments establish a critical role for the classical pathway, in this phenomenon. By contrast the role of the alternative pathway in maintaining complexes in solution was less important; only partial and delayed precipitation occurred in sera depleted of factor D (RD) or factor B (RB). B and D restored normal complement activity to depleted sera. No precipitation was detected in a reagent depleted of properdin (RP). The mechanisms of inhibition of precipitation are therefore distinct from those responsible for solubilization of an immune precipitate, which is largely dependent on the alternative pathway.
本研究使用放射性标记的牛血清白蛋白（BSA）和兔抗牛血清白蛋白，研究了补体介导的免疫沉淀抑制机制。纯化的酶原C1能够在反应的最初几分钟内使复合物保持可溶形式，而在纯化的C1q或C1 + 乙二胺四乙酸（EDTA）存在下，免疫沉淀立即发生。在C1q缺陷血清中，最初的免疫聚集之后是形成的沉淀物部分溶解，类似于在存在Mg EGTA的正常人血清中获得的情况。在C2缺陷血清中，沉淀以缓慢的速率发生。补充缺陷成分（分别为C1q或C2）可完全恢复对沉淀的抑制。这些实验确立了经典途径在这一现象中的关键作用。相比之下，替代途径在维持复合物处于溶液中的作用不太重要；在缺乏因子D（RD）或因子B（RB）的血清中仅发生部分和延迟的沉淀。B和D使耗尽的血清恢复正常补体活性。在缺乏备解素（RP）的试剂中未检测到沉淀。因此，沉淀抑制机制与负责免疫沉淀物溶解的机制不同，后者很大程度上依赖于替代途径。
