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• Platelet specific CD4+ T cells are required for anti-platelet antibody production. • Th1/Th2 immune deviation is directly implicated in ITP development and progression. • Th17 cells and platelets have multifaceted and pro-active mutual relationship. • Both numerical and functional abnormalities of Tregs were observed in ITP patients. • Th22, Th9 and Tfh cells could be also associated with ITP pathophysiology. Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by low platelet counts due to enhanced platelet clearance and compromised production. Traditionally, ITP was regarded a B cell mediated disorder as anti-platelet antibodies are detected in most patients. The very nature of self-antigens, evident processes of isotype switching and the affinity maturation of anti-platelet antibodies indicate that B cells in order to mount anti-platelet immune response require assistance of auto-reactive CD4+ T cells. For a long time, ITP pathogenesis has been exclusively reviewed through the prism of the disturbed balance between Th1 and Th2 subsets of CD4+ T cells, however, more recently new subsets of these cells have been described including Th17, Th9, Th22, T follicular helper and regulatory T cells. In this paper, we review the current understanding of the role and immunological mechanisms by which CD4+ T cells contribute to the pathogenesis of ITP. [ABSTRACT FROM AUTHOR]