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PD-1 blockade potentiates HIV latency reversal ex vivo in CD4+ T cells from ART-suppressed individuals
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PD-1 blockade potentiates HIV latency reversal ex vivo in CD4+ T cells from ART-suppressed individuals
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Journal Article
PD-1 blockade potentiates HIV latency reversal ex vivo in CD4+ T cells from ART-suppressed individuals
2019
Overview
HIV persists in latently infected CD4
+
T cells during antiretroviral therapy (ART). Immune checkpoint molecules, including PD-1, are preferentially expressed at the surface of persistently infected cells. However, whether PD-1 plays a functional role in HIV latency and reservoir persistence remains unknown. Using CD4
+
T cells from HIV-infected individuals, we show that the engagement of PD-1 inhibits viral production at the transcriptional level and abrogates T-cell receptor (TCR)-induced HIV reactivation in latently infected cells. Conversely, PD-1 blockade with the monoclonal antibody pembrolizumab enhances HIV production in combination with the latency reversing agent bryostatin without increasing T cell activation. Our results suggest that the administration of immune checkpoint blockers to HIV-infected individuals on ART may facilitate latency disruption.
The immune checkpoint molecule PD-1 is expressed on a fraction of CD4
+
T cells latently infected with HIV, but whether PD-1 plays a functional role in reservoir persistence remains unknown. Here, Fromentin et al. show that PD-1 blockade potentiates latency reversal ex vivo in CD4
+
T cells from ART suppressed individuals.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/31
/ 38/77
/ Antibodies, Monoclonal, Humanized - pharmacology
/ Antiretroviral Therapy, Highly Active
/ B7-H1 Antigen - pharmacology
/ CD4-Positive T-Lymphocytes - virology
/ HIV
/ Human immunodeficiency virus
/ Humanities and Social Sciences
/ Humans
/ Latency
/ Lymphocyte Activation - drug effects
/ Programmed Cell Death 1 Receptor - antagonists & inhibitors
/ Programmed Cell Death 1 Receptor - metabolism
/ Science
