Endogenous immune complexes present in sera from 10 different patients with systemic lupus erythematosus (SLE) in an active phase were allowed to bind to Raji cells; the ability of intact complement to release the cell-bound complexes from receptors was then examined. Fresh normal human serum, or, alternatively, zymosan-pretreated serum, was added to the complex-bearing Raji cells. Immune complexes remaining bound to Raji cell receptors after increasing times at 37 degrees C were quantitated by addition of 125I-labelled antiglobulin, after removal of serum by washing. In all 10 cases, complement-dependent release was observed. In parallel control studies performed under identical conditions, immune complexes prepared in vitro from bovine serum albumin (BSA) and guinea-pig anti-BSA antibody were used in place of the endogenous SLE complexes. The experimental complexes were released by fresh serum, but not by zymosan-treated serum, but not by zymosan-treated serum, when studied using either 125I-labelled anti-guinea-pig Ig or 125I-labelled complexes alone. The results suggest that intact complement can alter the immune complexes present in SLE sera and influence their interaction with receptors on lymphoid cells. The results further raise the possibility that hypocomplementaemia secondarily due to consumption of complement by immune complexes may contribute to the persistence of the complexes.