Delayed Expression of PD-1 and TIGIT on HIV-Specific CD8 T Cells in Untreated HLA-B*57:01 Individuals Followed from Early Infection.
CD4
CD8-positive T lymphocytes
HIV Gag
HIV-1
PD-1
T-cell immunoreceptor with Ig and ITIM domain
TIGIT
cellular immunity
disease progression
evolution
human HLA-B*5701 antigen
molecular evolution
programmed cell death protein 1
viral load
Journal
Journal of virology
ISSN: 1098-5514
Titre abrégé: J Virol
Pays: United States
ID NLM: 0113724
Informations de publication
Date de publication:
01 07 2020
01 07 2020
Historique:
received:
20
12
2019
accepted:
16
04
2020
pubmed:
1
5
2020
medline:
20
11
2020
entrez:
1
5
2020
Statut:
epublish
Résumé
While the relationship of protective human leukocyte antigen (HLA) class I alleles and HIV progression is well defined, the interaction of HLA-mediated protection and CD8 T-cell exhaustion is less well characterized. To gain insight into the influence of HLA-B*57:01 on the deterioration of CD8 T-cell responses during HIV infection in the absence of antiretroviral treatment, we compared HLA-B*57:01-restricted HIV-specific CD8 T-cell responses to responses restricted by other HLA class I alleles longitudinally after control of peak viremia. Detailed characterization of polyfunctionality, differentiation phenotypes, transcription factor, and inhibitory receptor expression revealed progression of CD8 T-cell exhaustion over the course of the infection in both patient groups. However, early effects on the phenotype of the total CD8 T-cell population were apparent only in HLA-B*57-negative patients. The HLA-B*57:01-restricted, HIV epitope-specific CD8 T-cell responses showed beneficial functional patterns and significantly lower frequencies of inhibitory receptor expression, i.e., PD-1 and coexpression of PD-1 and TIGIT, within the first year of infection. Coexpression of PD-1 and TIGIT was correlated with clinical markers of disease progression and declining percentages of the T-bet
Identifiants
pubmed: 32350076
pii: JVI.02128-19
doi: 10.1128/JVI.02128-19
pmc: PMC7343205
pii:
doi:
Substances chimiques
HLA-B Antigens
0
HLA-B*57:01 antigen
0
PDCD1 protein, human
0
Programmed Cell Death 1 Receptor
0
Receptors, Immunologic
0
TIGIT protein, human
0
Types de publication
Clinical Trial
Journal Article
Multicenter Study
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NCCIH NIH HHS
ID : K24 AT007827
Pays : United States
Organisme : NIAID NIH HHS
ID : P30 AI027763
Pays : United States
Organisme : NIAID NIH HHS
ID : P01 AI071713
Pays : United States
Informations de copyright
Copyright © 2020 Scharf et al.
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