University of Nis, Medical Faculty of Nis, Department of Immunology, Blvd. dr Zorana Djindjica 81, 18000 Nis, Serbia.
University of Nis, Medical Faculty of Nis, Department of Pathology, Blvd. dr Zorana Djindjica 81, 18000 Nis, Serbia.
Cell Immunol. 2020 May;351:104096. doi: 10.1016/j.cellimm.2020.104096. Epub 2020 Mar 14.
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增加和生成受损导致血小板计数降低。传统上，ITP 被认为是 B 细胞介导的疾病，因为大多数患者都检测到抗血小板抗体。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，B 细胞要产生抗血小板免疫反应，需要自身反应性 CD4 T 细胞的辅助。长期以来，ITP 的发病机制一直仅通过 CD4 T 细胞中 Th1 和 Th2 亚群之间失衡的视角进行审查，然而，最近这些细胞的新亚群已经被描述，包括 Th17、Th9、Th22、滤泡辅助 T 细胞和调节性 T 细胞。在本文中，我们回顾了目前对 CD4 T 细胞在 ITP 发病机制中的作用和免疫学机制的理解。
