Abstract
Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease characterized by autoantibody-mediated platelet destruction. Platelets with associated IgG are targeted for destruction by phagocytic cells bearing Fc receptors in the reticuloendothelial system. While there are a variety of therapeutics available for this incompletely understood disease, one of the treatments of choice is infusion of intravenous immunoglobulin (IVIG). This review will discuss the pathophysiology of ITP with an emphasis on the role of Fcgamma receptors in both the pathogenesis and treatment of the disease by IVIG. Other prominent theories of the mechanisms of action of IVIG, including the role of anti-idiotype antibodies, will also be addressed.
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