COMPLEMENT-MEDIATED INHIBITION OF IMMUNE PRECIPITATION .1. ROLE OF THE CLASSICAL AND ALTERNATIVE PATHWAYS

Abstract

The mechanisms involved in [human] complement(C)-mediated inhibition of immune precipitation was studied using radiolabeled BSA [bovine serum albumin] and rabbit anti-BSA. Purified proenzyme C1 was capable of maintaining the complexes in soluble form during the 1st few minutes of reaction; immune precipitation was immediate in the presence of purified C1q of C1 + EDTA. 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 or factor B. Factor B and factor D restored normal C activity to depleted sera. No precipitation was detected in a reagent depleted of properdin. 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.