Complement levels and circulating immune complexes in a controlled, longitudinal, multicentre study on effects of intravenous immunoglobulin in adults with AIDS-related complex/Walter-Reed 5. The ARC-IVIG Study Group.

The complement system, as the effector mechanism of the antigen-antibody reaction, and the levels of circulating immune complexes in a 1-year, double-blind, randomized, placebo-controlled study served as laboratory parameters to assess the effect of long-term high-dose intravenous immunoglobulin (IVIG) therapy in 30 adult patients (2 x 15) with AIDS-related complex/Walter-Reed 5 (ARC/WR5). We obtained no evidence of an adverse effect in such patients of high-dose IVIG administered over a 6-month period: none of the parameters studied showed a significant difference between the two groups of patients. In both groups, using data before the first infusion or using data of the whole study, a correlation between circulating immune complexes and classical complement pathway activation was found. The most striking increase was seen in the two groups of patients for functional serum factor D. The accumulation of serum factor D was not paralleled by an increase in serum creatinine. In patients with disease progressing from ARC to AIDS within the study period, an accumulation of serum factor D was not more or less pronounced than in those who remained in the ARC stage. Accumulation of factor D was not related to the clinical score as assessed in this study.

Solubilization of immune precipitates by complement in the absence of properdin or factor D.

Various experiments have demonstrated that immune precipitates (IPs) are not solubilized by complement in the absence of alternative pathway function. To determine whether the characteristics of the IPs were responsible for these observations, we studied the solubilization (Sol) of IPs formed by bovine serum albumin (BSA)-rabbit antiBSA and tetanus toxoid (TT)-human antiTT. Sera deficient in properdin solubilized a fraction of BSA-antiBSA precipitates, although only when the IPs were formed in antibody excess. The same sera solubilized TT-antiTT precipitates with some delay but almost as efficiently as normal serum. Factor D-depleted serum solubilized a fraction of TT-antiTT precipitates too, indicating that Sol may proceed through activation of the classical pathway only. Thus, the requirements for complement-mediated Sol depend on the characteristics of the IPs and do not necessarily include alternative pathway function.