Human T-lymphotropic virus type 1 (HTLV-1) and regulatory T cells in HTLV-1-associated neuroinflammatory disease.
Human T-lymphotropic virus type 1 (HTLV-1) and regulatory T cells in HTLV-1-associated neuroinflammatory disease.
复制标题
DOI：
10.3390/v3091532
复制
发表时间：
2011-09
期刊：
影响因子：
--
通讯作者：
Yamano Y
中科院分区：
文献类型：
--
作者：
Araya N;Sato T;Yagishita N;Ando H;Utsunomiya A;Jacobson S;Yamano Y
人类嗜T淋巴细胞病毒1型（HTLV-1）是一种逆转录病毒，是成人T细胞白血病/淋巴瘤（ATL）的病原体，并与多器官炎性疾病相关，包括HTLV-1相关的脊髓病/热带痉挛性下肢轻瘫（HAM/TSP）和葡萄膜炎。HTLV-1感染的T细胞已被假设为有助于这些疾病的发展，尽管确切的机制还不清楚。HTLV-1主要感染在适应性免疫应答中起核心作用的CD 4 + T辅助（Th）细胞。根据其功能、细胞因子分泌模式以及特异性转录因子和趋化因子受体的表达，从幼稚CD 4 + T细胞分化而来的Th细胞分为四个主要谱系：Th 1、Th 2、Th 17和T调节（Treg）细胞。CD 4 + CD 25 + CCR 4 + T细胞群主要由抑制性T细胞亚群组成，如健康个体中的Treg和Th 2亚群，是ATL和HAM/TSP患者中HTLV-1的主要病毒储库。有趣的是，在HAM/TSP患者中，CD 4 + CD 25 + CCR 4 + T细胞变成Th 1样细胞，如它们过量产生IFN-γ所证明的，这表明HTLV-1可以在细胞内诱导T细胞从Treg到IFN-γ+ T细胞的可塑性。本文综述了最近的研究HTLV-1和Treg细胞之间的关联，大大提高了对HTLV-1相关神经炎性疾病免疫失调的致病机制的理解。
Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus that is the causative agent of adult T cell leukemia/lymphoma (ATL) and associated with multiorgan inflammatory disorders, including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and uveitis. HTLV-1-infected T cells have been hypothesized to contribute to the development of these disorders, although the precise mechanisms are not well understood. HTLV-1 primarily infects CD4+ T helper (Th) cells that play a central role in adaptive immune responses. Based on their functions, patterns of cytokine secretion, and expression of specific transcription factors and chemokine receptors, Th cells that are differentiated from naïve CD4+ T cells are classified into four major lineages: Th1, Th2, Th17, and T regulatory (Treg) cells. The CD4+CD25+CCR4+ T cell population, which consists primarily of suppressive T cell subsets, such as the Treg and Th2 subsets in healthy individuals, is the predominant viral reservoir of HTLV-1 in both ATL and HAM/TSP patients. Interestingly, CD4+CD25+CCR4+ T cells become Th1-like cells in HAM/TSP patients, as evidenced by their overproduction of IFN-γ, suggesting that HTLV-1 may intracellularly induce T cell plasticity from Treg to IFN-γ+ T cells. This review examines the recent research into the association between HTLV-1 and Treg cells that has greatly enhanced understanding of the pathogenic mechanisms underlying immune dysregulation in HTLV-1-associated neuroinflammatory disease.