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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
- Source :
-
Clinical Immunology . Oct2008, Vol. 129 Issue 1, p132-144. 13p. - Publication Year :
- 2008
-
Abstract
- Abstract: 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)-α, but not IFN-γ, production. Inhibition of endocytosis, required for HIV-induced IFN-α production, prevented PDL-1 upregulation. IFN-α-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-α-dependent. IFN-α-receptor subunit 2 (IFNAR2), was expressed only by CCR5+ T cells and monocytes, explaining why these leukocytes responded to HIV-induced IFN-α. Finally, T cell proliferation was improved by PDL-1 blockade in HIV-treated PBMC. In the setting of HIV infection, IFN-α may negatively affect T cell responses by inducing PDL-1. [Copyright &y& Elsevier]
Details
- Language :
- English
- ISSN :
- 15216616
- Volume :
- 129
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Clinical Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 34379517
- Full Text :
- https://doi.org/10.1016/j.clim.2008.05.009