Complement behavior in infectious mononucleosis: possible mechanisms for the prevention of immune complex injury.
The acute-phase complement reaction was examined in patients with uncomplicated infectious mononucleosis (IM). Concentrations of both complement and complement inhibitor protein were significantly elevated during the acute phase, and turnover studies with purified 125I-labeled C3 showed this increase to result from increased C3 synthesis. Nine of 16 patients had evidence of in vivo complement activation during this period. Despite high levels of C1q-binding immune complexes in most acute-phase sera from patients with IM, the capacity of these sera to solubilize immune precipitates in vitro was normal. In contrast, four of five sera from patients with active systemic lupus erythematosus showed reduced solubilization. The level of C3b inactivator in sera from patients with IM and the percentage conversion of C3 after in vitro complement activation by aggregated IgG were inversely correlated (P less than 0.01). It is proposed that an acute-phase complement reaction limits immune complex-mediated injury to tissue by maintaining those complement functions that are required for the effective processing of circulating antigen/antibody material.
D000293:Adolescent; D000328:Adult; D000936:Antigen-Antibody Complex; D003167:Complement Activation; D003176:Complement C3 / Q000378:metabolism; D003180:Complement C3b Inactivator Proteins / Q000097:blood; D003165:Complement System Proteins / Q000378:metabolism*; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007244:Infectious Mononucleosis / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology
D000936:Antigen-Antibody Complex; D003176:Complement C3; D003180:Complement C3b Inactivator Proteins; D007074:Immunoglobulin G; D003165:Complement System Proteins