Division of Rheumatology, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA.
Division of Infectious Diseases, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
Virology. 2018 Mar;516:21-29. doi: 10.1016/j.virol.2017.12.036. Epub 2018 Jan 8.
During chronic HIV-1 infection, regulatory CD4 T cells (Tregs) frequently represent the largest subpopulation of CD4 T cell subsets, implying relative resistant to HIV-1. When HIV-1 infection of CD4 T cells was explored in vitro and ex vivo from patient samples, Tregs possessed lower levels of HIV-1 DNA and RNA in comparison with conventional effector and memory CD4 T cells. Moreover, Tregs suppressed HIV-1 expression in other CD4 T cells in an in vitro co-culture system. This suppression was mediated in part via multiple inhibitory surface proteins expressed on Tregs. Antibody blockade of CTLA-4, PD-1, and GARP on Tregs resulted in increased HIV-1 DNA integration and mRNA expression in neighboring CD4 T cells. Moreover, antibody blockade of Tregs inhibitory proteins resulted in increased HIV-1 LTR transcription in co-cultured CD4 T cells. Thus, Tregs inhibit HIV-1 infection of other CD4 T cell subsets via interactions with inhibitory cell surface proteins.
在慢性 HIV-1 感染期间,调节性 CD4 T 细胞(Tregs)通常代表 CD4 T 细胞亚群中最大的亚群,这意味着它们对 HIV-1 具有相对抗性。当在体外和来自患者样本的体外探索 HIV-1 对 CD4 T 细胞的感染时,与传统效应器和记忆 CD4 T 细胞相比,Tregs 中 HIV-1 DNA 和 RNA 的水平较低。此外,Tregs 在体外共培养系统中抑制其他 CD4 T 细胞中的 HIV-1 表达。这种抑制部分是通过 Tregs 上表达的多种抑制性表面蛋白介导的。抗体阻断 Tregs 上的 CTLA-4、PD-1 和 GARP,导致相邻 CD4 T 细胞中 HIV-1 DNA 整合和 mRNA 表达增加。此外,抗体阻断 Tregs 的抑制蛋白导致共培养的 CD4 T 细胞中 HIV-1 LTR 转录增加。因此,Tregs 通过与抑制性细胞表面蛋白相互作用抑制其他 CD4 T 细胞亚群中的 HIV-1 感染。