THE production of antiplatelet antibodies and removal of IgG-coated platelets by the mononuclear phagocyte system play an important part in the pathogenesis of immune thrombocytopenic purpura. The coating of platelets with immunoglobulin results in their removal in the spleen and liver, presumably by receptors for the Fc fragment of IgG (Fcγ).^{1 , 2} Prolongation of Fcγ-receptor-mediated clearance of opsonized red cells after splenectomy^{1 , 3} and infusions of high doses of intravenous gamma globulin,^{4 , 5} in conjunction with favorable clinical responses to these therapies, support this hypothesis. Some patients, however, respond to neither of these treatments nor to other, less specific forms of immunosuppression, such . . .