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CD4(+) T cell phenotypes in the pathogenesis of immune thrombocytopenia

机译：免疫血小板减少症发病机制中的CD4（+）T细胞表型

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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.
机译：免疫血小板减少症（ITP）是一种自身免疫性疾病，其特征在于由于血小板间隙增强和损害的生产而具有低血小板计数。 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检测到抗血小板抗体。 自我抗原的本质，同种型切换的明显过程和抗血小板抗体的亲和力成熟表明B细胞为了安装抗血小板免疫应答，需要辅助自动活性CD4（+）T细胞。 长期以来，通过CD4（+）T细胞Th1和Th2子集之间的受干扰平衡的棱镜专门审查了ITP发病机制，然而，已经描述了这些细胞的最近新子集，包括Th17，Th9，Th22， T卵泡助剂和调节性T细胞。 在本文中，我们审查了目前对CD4（+）T细胞有助于ITP发病机制的作用和免疫机制的理解。

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