SUMMARYWe investigated the increase of platelet-associated IgG and complement eomponent 3 (C'O caused by the in vitro action of anti-platelet MoAbs, and the effect of mouse and human IgG on these events, Anti-glycoprotein Ilb/Illa and anti-glycoprotein Ib MoAbs caused ii slight increase of C-,. but not of platelet-associated IgG. In contrast. anti-CD9andanti-Fc-; II receptor MoAbs caused an increase of both platelct-assoeiated Ci and IgG, In particular, three MoAbs which activated the complement system caused a marked increase of Ci. When platelet-rich plasma was treated with aspirin and prostaglandin E| before incubation with antibodies, the increase of pUitelet-associated IgG was inhibited in all cases. In contrast, the inerease of platelet-associated Ci was scarcely inllucnced. These results suggest that the binding to platelets of platelet-activating antibodies caused the inereased expression of~IgG molecules on thcpialetet surface and a possible increase ofpiatelct-associated [gG, However, the inerease of platelet-associated Ci appeared to depend on specific eharacteristies cf the antibodies tested, such as a eomplcment-activiiting elTect. In addition, intact mouse or human IgG inhibited the increase of platelet-assoeiated Ci caused by complement-aetivating antibodies, white F(ab')i mouse or human IgG had no such effect. This suggested that the Fc portion of IgG may block the increase of Cy mediated by anti-platelet antibodies.