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231223s2008 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2008.05.009
|2 doi
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|a pubmed24n0604.xml
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|a (DE-627)NLM181121018
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|a (NLM)18650129
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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1 |
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|a Boasso, Adriano
|e verfasserin
|4 aut
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1 |
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|a PDL-1 upregulation on monocytes and T cells by HIV via type I interferon
|b restricted expression of type I interferon receptor by CCR5-expressing leukocytes
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|c 2008
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 07.10.2008
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|a Date Revised 20.10.2021
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a 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
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|a Journal Article
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650 |
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|a Research Support, N.I.H., Intramural
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650 |
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|a Antigens, CD
|2 NLM
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|a B7-1 Antigen
|2 NLM
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|a B7-2 Antigen
|2 NLM
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7 |
|a B7-H1 Antigen
|2 NLM
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650 |
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|a CD274 protein, human
|2 NLM
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|a IFNAR2 protein, human
|2 NLM
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|a Interferon Type I
|2 NLM
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|a Receptors, CCR5
|2 NLM
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|a Toll-Like Receptors
|2 NLM
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7 |
|a Receptor, Interferon alpha-beta
|2 NLM
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|a 156986-95-7
|2 NLM
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700 |
1 |
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|a Hardy, Andrew W
|e verfasserin
|4 aut
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700 |
1 |
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|a Landay, Alan L
|e verfasserin
|4 aut
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700 |
1 |
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|a Martinson, Jeffrey L
|e verfasserin
|4 aut
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700 |
1 |
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|a Anderson, Stephanie A
|e verfasserin
|4 aut
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700 |
1 |
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|a Dolan, Matthew J
|e verfasserin
|4 aut
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700 |
1 |
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|a Clerici, Mario
|e verfasserin
|4 aut
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700 |
1 |
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|a Shearer, Gene M
|e verfasserin
|4 aut
|
773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 129(2008), 1 vom: 15. Okt., Seite 132-44
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
|
773 |
1 |
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|g volume:129
|g year:2008
|g number:1
|g day:15
|g month:10
|g pages:132-44
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856 |
4 |
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|u http://dx.doi.org/10.1016/j.clim.2008.05.009
|3 Volltext
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_11
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|a GBV_ILN_24
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912 |
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|a GBV_ILN_350
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951 |
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|a AR
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|d 129
|j 2008
|e 1
|b 15
|c 10
|h 132-44
|