T cells in the pathogenesis of immune thrombocytopenia

Abstract

Immune thrombocytopenia (ITP) is an acquired autoimmune bleeding disease characterized by both increased platelet destruction and reduced platelet production. ITP involves complicated upstream immune dysregulations in which T-cell subsets are supposed to take the center stage. Survival of autoreactive T cells is prolonged. Th-cell polarization is observed in Th1, Th17, and Th22 subsets with a positive correlation, whereas Tregs, a protective subset, is deficient in both frequency and function. Restoration of the imbalanced Th1/Th17/Tregs may correct the abnormal autoimmunity. T-follicular helper cells (TFH) are recently found to regulate antiplatelet–antibody production in ITP. Autoreactive CD8+ T cells mediate direct lysis of platelets and according to our latest study, participate in desialylation and hepatic clearance of platelets. Future studies need to identify definite targets for management of ITP.