Immune reactions in infective endocarditis. II. Relevance of circulating immune complexes, serum inhibition factors, lymphocytotoxic reactions, and antibody-dependent cellular cytotoxicity against cardiac target cells.

Circulating immune complexes (IC) were detected in 35 out of 41 patients (85%) with infective endocarditis of known bacterial origin in contrast to only 9 out of 20 patients (45%) with endocarditis but negative blood cultures (p less than 0.05). Peak IC levels of 33.25 +/- 24.33 micrograms/ml in the early period fell significantly to 8.38 +/- 13.37 micrograms/ml after antibiotic treatment (p less than 0.001). High levels of IC coincided with relative hypocomplementemia. Erythrocyturia was observed in 51 of 58 IC-positive patients demonstrating peripheral sequelae of circulating IC. Incidence and concentrations of IC correlated neither with the mere presence of the rheumatoid factor nor with the titers of antimyolemmal antibodies, nor with antibody mediated cytolysis in the presence of complement. Serum inhibition factors (SIF) and E-rosette inhibitory factors (RIF) were not demonstrated, indicating that IC in endocarditis do not suppress phytohemagglutinin-induced lymphocyte proliferation or the E-rosetting of T cells. Significant lymphocytotoxicity against heterologous cardiac target cells without serum (LC) could be demonstrated in 11 out of 23 patients (48%) with endocarditis as compared to its absence in controls (n = 33, p less than 0.01). In assays of antibody-dependent cellular cytotoxicity (ADCC), either enhancement or blocking of lymphocytotoxicity by autologous serum or both was observed. The modulation of lymphocytotoxicity was most likely due to antimyolemmal antibodies, to IC, or to both, although effects of other serum factors cannot be ruled out completely.