Anti-D: mechanisms of action.

Immunoglobulin that recognizes and binds specifically to the erythrocyte D antigen (anti-D globulin, WinRho SDF; Nabi, Boca Raton, FL) has recently been shown to be an effective therapy for many patients with idiopathic thrombocytopenic purpura (ITP). Its mechanisms of action are not completely understood. Intravenous (IV) infusion of anti-D into a D-positive recipient leads to antibody coating of circulating erythrocytes that are cleared primarily by the spleen. This immune-mediated clearance of sensitized erythrocytes occupies the reticuloendothelial system and allows survival of antibody-coated platelets. Based on clinical observations, experimental data, and theoretical calculations, the efficacy of anti-D therapy in ITP depends on several factors that influence the amount of erythrocyte sensitization and the rate of immune-mediated erythrocyte clearance by the spleen. Antibody characteristics, including the antibody concentration, binding affinity, and dissociation constants, may be important, as well as the number of D-antigen binding sites on the erythrocytes. Although the primary mechanism of action of anti-D is believed to be immunologic blockade of Fc receptors (FcR) within the reticuloendothelial system (RES), other immunomodulatory effects are also possible.