TIM-3 and Its Immunoregulatory Role in HIV Infection
TIM-3 and Its Immunoregulatory Role in HIV Infection
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DOI：
10.4172/2155-9899.s7-007
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发表时间：
2013
期刊：
影响因子：
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通讯作者：
A. Rahman;K. Clayton;S. Mujib;I. Fong;M. Ostrowski
中科院分区：
文献类型：
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作者：
A. Rahman;K. Clayton;S. Mujib;I. Fong;M. Ostrowski
人类免疫缺陷病毒1型（HIV）感染的慢性性质导致HIV特异性CD 8 + T细胞的功能耗尽。尽管到目前为止已经鉴定了多种耗竭标志物，但最近发现的T细胞免疫球蛋白和粘蛋白结构域3（TIM-3）分子区分真正耗竭的T细胞与复制性衰老和功能损伤。TIM-3在慢性HIV感染期间表达于T辅助1型（TH 1）和T细胞毒性1型（TC 1）T细胞上，并且一旦与其配体连接就传递负信号以阻止T细胞功能。TIM-3连接的这种负面作用可以被利用为我们的优势，作为治疗HIV感染个体的治疗方法。除了耗竭，TIM-3表达的改变还与自身免疫和耐受性消除有关。
The chronic nature of Human Immunodeficiency Virus Type 1 (HIV) infection leads to the functional exhaustion of HIV specific CD8+ T cells. Although multiple markers of exhaustion have been identified so far, the recently discovered T cell immunoglobulin and mucin domain 3 (TIM-3) molecules distinguishes bona fide exhausted T cells with replicative senescence and functional impairment. TIM-3 is expressed on T helper type 1 (TH1) and T cytotoxic type 1 (TC1) T cells during chronic HIV infection and once ligated to its ligand transmits negative signaling to arrest T cell function. This negative effect of TIM-3 ligation could be exploited to our advantage as a therapeutic approach to treat HIV-infected individuals. In addition to exhaustion, altered TIM-3 expression has been implicated in autoimmunity and tolerance abrogation.