During the past few decades a number of studies has described T cell defects and attempted to elucidate their role in the pathogenesis of idiopathic thrombocytopenic purpura (ITP). Some studies implicate T cells as potential initiators of autoantibody production in ITP. However, only a few of these have studied the role that the T cell receptor may play in the pathogenesis of ITP. In a variety of autoimmune syndromes interest has focused on the alpha- and beta-chains of the T cell receptor. Deviations from the normal T cell receptor gene usage have been reported in rheumatoid arthritis, systemic lupus erythaematosus and multiple sclerosis. Usually, these studies have shown a restricted heterogeneity of T cell receptor variable gene usage. The studies on the T cell receptor in ITP have included a limited number of patients, which makes it difficult to evaluate the significance of the role that the T cell receptor may play in the pathogenesis of ITP. Further studies are warranted.
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