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.

免疫性血小板减少症（ITP）是一种自身免疫性疾病，其特征是由于血小板清除率提高和生产受到损害，血小板计数低。传统上，ITP被认为是B细胞介导的疾病，因为在大多数患者中都检测到了抗血小板抗体。自身抗原的本质，同种型转换的明显过程以及抗血小板抗体的亲和力成熟表明，为了进行抗血小板免疫反应，B细胞需要自身反应性CD4 ⁺ T细胞的协助。长期以来，ITP发病机理一直是通过CD4 ^+的Th1和Th2子集之间的平衡失衡来专门研究的T细胞，但是，最近已经描述了这些细胞的新子集，包括Th17，Th9，Th22，T卵泡辅助细胞和调节性T细胞。在本文中，我们综述了当前对CD4 ⁺ T细胞对ITP发病机理的作用和免疫机制的理解。