Department of Microbial Pathogenesis and Immunology, Texas A&M University Health Science Center, Bryan, TX 77807, USA.
Department of Ophthalmology, Harvard University School of Medicine, Boston, MA 02215, USA.
Viruses. 2021 Apr 25;13(5):753. doi: 10.3390/v13050753.
The viral antigen (Ag)-specific CD8+ cytotoxic T lymphocytes (CTLs) derived from pluripotent stem cells (PSCs), i.e., PSC-CTLs, have the ability to suppress the human immunodeficiency virus (HIV) infection. After adoptive transfer, PSC-CTLs can infiltrate into the local tissues to suppress HIV replication. Nevertheless, the mechanisms by which the viral Ag-specific PSC-CTLs elicit the antiviral response remain to be fully elucidated. In this study, we generated the functional HIV-1 Gag epitope SL9-specific CTLs from the induced PSC (iPSCs), i.e., iPSC-CTLs, and investigated the suppression of SL9-specific iPSC-CTLs on viral replication and the protection of CD4+ T cells. A chimeric HIV-1, i.e., EcoHIV, was used to produce HIV replication in mice. We show that adoptive transfer of SL9-specific iPSC-CTLs greatly suppressed EcoHIV replication in the peritoneal macrophages and spleen in the animal model. Furthermore, we demonstrate that the adoptive transfer significantly reduced expression of PD-1 on CD4+ T cells in the spleen and generated persistent anti-HIV memory T cells. These results indicate that stem cell-derived viral Ag-specific CTLs can robustly accumulate in the local tissues to suppress HIV replication and prevent CD4+ T cell exhaustion through reduction of PD-1 expression.
源自多能干细胞(PSCs)的病毒抗原(Ag)特异性 CD8+细胞毒性 T 淋巴细胞(CTLs),即 PSC-CTLs,具有抑制人类免疫缺陷病毒(HIV)感染的能力。过继转移后,PSC-CTLs 可以浸润到局部组织中抑制 HIV 复制。然而,病毒 Ag 特异性 PSC-CTLs 引发抗病毒反应的机制仍有待充分阐明。在这项研究中,我们从诱导多能干细胞(iPSCs)中产生了功能性 HIV-1 Gag 表位 SL9 特异性 CTLs,即 iPSC-CTLs,并研究了 SL9 特异性 iPSC-CTLs 对病毒复制的抑制作用和对 CD4+T 细胞的保护作用。使用嵌合 HIV-1,即 EcoHIV,在小鼠中产生 HIV 复制。我们表明,SL9 特异性 iPSC-CTLs 的过继转移可显著抑制动物模型中腹腔巨噬细胞和脾脏中的 EcoHIV 复制。此外,我们证明过继转移可显著降低脾脏中 CD4+T 细胞上 PD-1 的表达,并产生持续的抗 HIV 记忆 T 细胞。这些结果表明,源自干细胞的病毒 Ag 特异性 CTLs 可以在局部组织中大量积累,抑制 HIV 复制,并通过降低 PD-1 表达来防止 CD4+T 细胞衰竭。