PDL-1 upregulation on monocytes and T cells by HIV via type I interferon restricted expression of type I interferon receptor by CCR5-expressing leukocytes

PDL-1 upregulation on monocytes and T cells by HIV via type I interferon : restricted expression of type I interferon receptor by CCR5-expressing leukocytes

The programmed death (PD)-1 interacts with its ligand (PDL-1) delivering a negative signal to T cells. During human immunodeficiency virus (HIV)-1 infection PD-1 and PDL-1 expressions are increased. Here we show that monocytes and CCR5(+) T cells of HIV-uninfected donors upregulated PDL-1 upon in vi...

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Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 129(2008), 1 vom: 15. Okt., Seite 132-44
1. Verfasser: Boasso, Adriano (VerfasserIn)
Weitere Verfasser: Hardy, Andrew W, Landay, Alan L, Martinson, Jeffrey L, Anderson, Stephanie A, Dolan, Matthew J, Clerici, Mario, Shearer, Gene M
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2008
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, N.I.H., Intramural Antigens, CD B7-1 Antigen B7-2 Antigen B7-H1 Antigen CD274 protein, human IFNAR2 protein, human Interferon Type I Receptors, CCR5 mehr... Toll-Like Receptors Receptor, Interferon alpha-beta 156986-95-7
Beschreibung
Zusammenfassung:The programmed death (PD)-1 interacts with its ligand (PDL-1) delivering a negative signal to T cells. During human immunodeficiency virus (HIV)-1 infection PD-1 and PDL-1 expressions are increased. Here we show that monocytes and CCR5(+) T cells of HIV-uninfected donors upregulated PDL-1 upon in vitro exposure to HIV. HIV-induced PDL-1 required interferon (IFN)-alpha, but not IFN-gamma, production. Inhibition of endocytosis, required for HIV-induced IFN-alpha production, prevented PDL-1 upregulation. IFN-alpha-inducing Toll-like receptor (TLR) agonists increased PDL-1 on monocytes and CCR5(+) T cells. CD80 and CD86 were also increased on monocytes and CCR5(+) T cells after HIV exposure, but only CD80 was IFN-alpha-dependent. IFN-alpha-receptor subunit 2 (IFNAR2), was expressed only by CCR5(+) T cells and monocytes, explaining why these leukocytes responded to HIV-induced IFN-alpha. Finally, T cell proliferation was improved by PDL-1 blockade in HIV-treated PBMC. In the setting of HIV infection, IFN-alpha may negatively affect T cell responses by inducing PDL-1
Beschreibung:Date Completed 07.10.2008
Date Revised 29.05.2025
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2008.05.009