Division of Microbiology and Immunology, Yerkes National Primate Research Center, Emory University; Atlanta, Georgia, United States of America.
Barrier Immunity Section, Laboratory of Viral Diseases, NIAID, NIH; Bethesda, Maryland, United States of America.
PLoS Pathog. 2022 Jul 22;18(7):e1010723. doi: 10.1371/journal.ppat.1010723. eCollection 2022 Jul.
Despite the advent of effective antiretroviral therapy (ART), human immunodeficiency virus (HIV) continues to pose major challenges, with extensive pathogenesis during acute and chronic infection prior to ART initiation and continued persistence in a reservoir of infected CD4 T cells during long-term ART. CD101 has recently been characterized to play an important role in CD4 Treg potency. Using the simian immunodeficiency virus (SIV) model of HIV infection in rhesus macaques, we characterized the role and kinetics of CD101+ CD4 T cells in longitudinal SIV infection. Phenotypic analyses and single-cell RNAseq profiling revealed that CD101 marked CD4 Tregs with high immunosuppressive potential, distinct from CD101- Tregs, and these cells also were ideal target cells for HIV/SIV infection, with higher expression of CCR5 and α4β7 in the gut mucosa. Notably, during acute SIV infection, CD101+ CD4 T cells were preferentially depleted across all CD4 subsets when compared with their CD101- counterpart, with a pronounced reduction within the Treg compartment, as well as significant depletion in mucosal tissue. Depletion of CD101+ CD4 was associated with increased viral burden in plasma and gut and elevated levels of inflammatory cytokines. While restored during long-term ART, the reconstituted CD101+ CD4 T cells display a phenotypic profile with high expression of inhibitory receptors (including PD-1 and CTLA-4), immunsuppressive cytokine production, and high levels of Ki-67, consistent with potential for homeostatic proliferation. Both the depletion of CD101+ cells and phenotypic profile of these cells found in the SIV model were confirmed in people with HIV on ART. Overall, these data suggest an important role for CD101-expressing CD4 T cells at all stages of HIV/SIV infection and a potential rationale for targeting CD101 to limit HIV pathogenesis and persistence, particularly at mucosal sites.
尽管出现了有效的抗逆转录病毒疗法 (ART),但人类免疫缺陷病毒 (HIV) 仍然带来了重大挑战,在开始 ART 之前的急性和慢性感染期间,其广泛的发病机制以及在长期 ART 期间,在受感染的 CD4 T 细胞库中持续存在。最近已经确定 CD101 在 CD4 Treg 效力中发挥重要作用。我们使用猕猴 HIV 感染的猴免疫缺陷病毒 (SIV) 模型,描述了 CD101+ CD4 T 细胞在纵向 SIV 感染中的作用和动力学。表型分析和单细胞 RNAseq 分析揭示,CD101 标记具有高免疫抑制潜力的 CD4 Tregs,与 CD101- Tregs 不同,这些细胞也是 HIV/SIV 感染的理想靶细胞,在肠道黏膜中具有更高的 CCR5 和 α4β7 表达。值得注意的是,在急性 SIV 感染期间,与 CD101- 对应物相比,所有 CD4 亚群中 CD101+ CD4 T 细胞均优先耗尽,Treg 区显著减少,黏膜组织也显著减少。CD101+ CD4 的耗竭与血浆和肠道中的病毒载量增加以及炎症细胞因子水平升高有关。虽然在长期 ART 期间得到恢复,但重建的 CD101+ CD4 T 细胞显示出高表达抑制性受体(包括 PD-1 和 CTLA-4)、免疫抑制细胞因子产生和高 Ki-67 水平的表型特征,这与稳态增殖的潜力一致。在接受 ART 的 HIV 感染者中,SIV 模型中发现的 CD101+ 细胞的耗竭和这些细胞的表型特征得到了证实。总体而言,这些数据表明 CD101 表达的 CD4 T 细胞在 HIV/SIV 感染的各个阶段都起着重要作用,靶向 CD101 以限制 HIV 发病机制和持续性,特别是在黏膜部位,具有潜在的合理性。