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基于 PD-1 的疫苗接种后，SHIVSF162P3CN 回忆性效应记忆 CD8+ T 细胞持续抑制病毒血症。

Sustained viremia suppression by SHIVSF162P3CN-recalled effector-memory CD8+ T cells after PD1-based vaccination.

机构信息

AIDS Institute, Department of Microbiology, State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong SAR, China.

HKU-AIDS Institute Shenzhen Research Laboratory and AIDS Clinical Research Laboratory, Guangdong Key Laboratory of Emerging Infectious Diseases, Shenzhen Key Laboratory of Infection and Immunity, Shenzhen Third People's Hospital, Shenzhen, China.

出版信息

PLoS Pathog. 2021 Jun 14;17(6):e1009647. doi: 10.1371/journal.ppat.1009647. eCollection 2021 Jun.

DOI:10.1371/journal.ppat.1009647
PMID:34125864
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8202916/
Abstract

HIV-1 functional cure requires sustained viral suppression without antiretroviral therapy. While effector-memory CD8+ T lymphocytes are essential for viremia control, few vaccines elicit such cellular immunity that could be potently recalled upon viral infection. Here, we investigated a program death-1 (PD1)-based vaccine by fusion of simian immunodeficiency virus capsid antigen to soluble PD1. Homologous vaccinations suppressed setpoint viremia to undetectable levels in vaccinated macaques following a high-dose intravenous challenge by the pathogenic SHIVSF162P3CN. Poly-functional effector-memory CD8+ T cells were not only induced after vaccination, but were also recalled upon viral challenge for viremia control as determined by CD8 depletion. Vaccine-induced effector memory CD8+ subsets displayed high cytotoxicity-related genes by single-cell analysis. Vaccinees with sustained viremia suppression for over two years responded to boost vaccination without viral rebound. These results demonstrated that PD1-based vaccine-induced effector-memory CD8+ T cells were recalled by AIDS virus infection, providing a potential immunotherapy for functional cure.

摘要

HIV-1 功能性治愈需要在没有抗逆转录病毒治疗的情况下持续抑制病毒。虽然效应记忆 CD8+T 淋巴细胞对于控制病毒血症至关重要，但很少有疫苗能引发如此强烈的细胞免疫反应，以便在病毒感染时能够有效地被召回。在这里，我们研究了一种基于程序性死亡受体 1（PD1）的疫苗，它将猴免疫缺陷病毒衣壳抗原与可溶性 PD1 融合。同源疫苗接种可在高剂量静脉内挑战致病性 SHIVSF162P3CN 后，将接种猕猴的设定点病毒血症抑制到无法检测的水平。不仅在接种疫苗后诱导了多功能效应记忆 CD8+T 细胞，而且在病毒挑战后也被召回以控制病毒血症，这可以通过 CD8 耗竭来确定。通过单细胞分析，疫苗诱导的效应记忆 CD8+T 细胞亚群显示出高细胞毒性相关基因。两年多来持续抑制病毒血症的疫苗接种者在加强接种后没有出现病毒反弹。这些结果表明，艾滋病病毒感染会召回 PD1 为基础的疫苗诱导的效应记忆 CD8+T 细胞，为功能性治愈提供了一种潜在的免疫疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/4c7a0b0d4831/ppat.1009647.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/fb91421c9a14/ppat.1009647.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/50754a3bfdb6/ppat.1009647.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/3aad571f49b6/ppat.1009647.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/3c0bf2da9352/ppat.1009647.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/5385f7c1d2e3/ppat.1009647.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/4c7a0b0d4831/ppat.1009647.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/fb91421c9a14/ppat.1009647.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/50754a3bfdb6/ppat.1009647.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/3aad571f49b6/ppat.1009647.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/3c0bf2da9352/ppat.1009647.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/5385f7c1d2e3/ppat.1009647.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab1f/8202916/4c7a0b0d4831/ppat.1009647.g006.jpg

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