Inhibition of Autoantibody Binding to Platelet Glycoprotein lib/Illa by Anti-Idiotypic Antibodies in Intravenous Gammaglobulin

Intravenous immunoglobulin (lVlgG) causes an acute rise in the platelet count in the majority of patients with chronic immune thrombocytopenic purpura (ITP) but the mechanism(s) of action is still unknown. We evaluated the ability of three different IVIgG preparations to inhibit the in vitro binding of autoantibody to platelet glycoprotein (GP) llb/ lila. ITP plasma. known to contain anti-GPIIb/Illa antibodies, was incubated overnight with either lVlgG or bovine serum albumin (BSA) followed by measurement of the autoantibody titer. Binding of autoantibody from eight ITP patients was inhibited by lVIgG in proportion to the lVlgG concentration. Using 3.2% lVigG. compatible with therapeutic concentrations expected in vivo. mean inhibition of autoantibody binding ranged from 20.2% to 41 .3%. No inhibition by IVIgG of alloantibody binding to the same or