Immune thrombocytopenia (ITP) is an autoimmune disease, characterized by increased bleeding due to a reduced platelet count. The pathogenesis of ITP is very complex and involves autoantibody production and T-cell-mediated immune abnormalities. An imbalance of effector and regulatory CD4 T cells and the breach of tolerance primarily cause ITP, leading to the dysfunctional development of autoreactive Th cells (including Th1, Th2, and Th17 cells) and Tregs. The loss of auto-platelet antigen tolerance in ITP results in autoantibody- and cytotoxic T-cell-mediated platelet clearance. T-cell-related genetic risk factors significantly influence the development and progression of this disease. New therapies targeting T cells have emerged as potentially effective cures for this disease. This review summarizes the role of T cells in ITP.
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