When platelets that are AB0-nonidentical are transfused, circulating immune complexes (CIC) are formed. In the present study we examined the ability of polyclonal antibodies to two C1q receptors on platelets, cC1q-R and gC1q-R, and a monoclonal IgG Fc gamma RII (CD32) antibody directed against the platelet Fc receptor to inhibit the uptake of CIC involving the AB0 blood group system by normal platelets. Four types of immune complexes of varying purity were made in vitro. In addition serum from 5 refractory group A patients who had demonstrable AB0 CIC, 5 patients who had received only AB0-identical platelets and had no AB0 CIC and 6 normal donors were evaluated. After exposure of normal platelets to serum of patients with demonstrable AB0 CIC there were increased levels of platelet-associated IgG. This binding was partially inhibited by preincubation of the platelets with either anti-cC1q-R (3/5 patients), gC1q-R (3/5 patients) or IgG Fc gamma RII in 4/5 patients. However, the pattern of inhibition by the three antibodies was variable. Using the artificial immune complexes a more consistent pattern was obtained. The binding of four types of artificial immune complexes to platelets was reduced by 67-99% after preincubation of the platelets with antibodies to the complement and Fc receptors. The present work supports the hypothesis that AB0 CIC bind to Fc and complement receptors on the platelet and if confirmed would suggest a pathophysiological mechanism for the clinical observations of the important role of AB0 in platelet transfusion.