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细胞亚群的最大亚群，这意味着其对HIV-1的相对耐药性。当从患者样本中进行体外和离体研究HIV-1感染CD4 T细胞时，与传统的效应和记忆CD4 T细胞相比，Tregs的HIV-1 DNA和RNA含量较低。此外，在体外，Tregs抑制了其他CD4 T细胞中HIV-1的表达共培养系统。这种抑制作用部分是通过在Tregs上表达的多种抑制性表面蛋白介导的。抗体对Tregs的CTLA-4，PD-1和GARP的阻断导致HIV-1 DNA整合和邻近CD4 T细胞中mRNA表达的增加。此外，抗体对Tregs抑制蛋白的阻断导致在共培养的CD4 T细胞中HIV-1 LTR转录增加。因此，Treg通过与抑制性细胞表面蛋白的相互作用抑制HIV-1感染其他CD4 T细胞亚群。