Influence of HLA-C environment on the spontaneous clearance of hepatitis C in European HIV-HCV co-infected individuals.
Adult
Cells, Cultured
Coinfection
/ immunology
Female
Flow Cytometry
/ methods
France
Genotype
HIV Infections
/ immunology
HLA-C Antigens
/ genetics
Hepatitis C
/ immunology
Humans
Killer Cells, Natural
/ immunology
Male
Middle Aged
Receptors, KIR
/ genetics
Receptors, KIR2DL1
/ genetics
Receptors, KIR2DL2
/ genetics
Receptors, KIR2DL3
/ genetics
Remission, Spontaneous
T-Lymphocyte Subsets
/ immunology
HLA
KIR
co-infection
hepatitis C
spontaneous clearance
Journal
Clinical and experimental immunology
ISSN: 1365-2249
Titre abrégé: Clin Exp Immunol
Pays: England
ID NLM: 0057202
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
05
08
2020
revised:
07
12
2020
accepted:
07
12
2020
pubmed:
15
12
2020
medline:
28
9
2021
entrez:
14
12
2020
Statut:
ppublish
Résumé
Natural killer (NK) cell functions are regulated by diverse inhibitory and activating receptors, including killer cell immunoglobulin-like receptors (KIR), which interact with human leukocyte antigen (HLA) class I molecules. Some KIR/HLA genetic combinations were reported associated with spontaneous clearance (SC) of hepatitis C virus (HCV) but with discordant results, possibly reflecting KIR and/or HLA gene polymorphism according to populations. KIR/HLA genetic combinations associated with both an exhaustive NK and T cell repertoire were investigated in a cohort of HIV-HCV co-infected individuals with either SC (n = 68) or chronic infection (CI, n = 163) compared to uninfected blood donors [controls (Ctrl), n = 100]. Multivariate analysis showed that the HLA C2C2 environment was associated with SC only in European HIV-HCV co-infected individuals [odds ratio (OR) = 4·30, 95% confidence interval = 1·57-12·25, P = 0·005]. KIR2D
Identifiants
pubmed: 33314121
doi: 10.1111/cei.13562
pmc: PMC7944354
doi:
Substances chimiques
HLA-C Antigens
0
KIR2DL1 protein, human
0
KIR2DL2 protein, human
0
KIR2DS1 protein, human
0
Receptors, KIR
0
Receptors, KIR2DL1
0
Receptors, KIR2DL2
0
Receptors, KIR2DL3
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
107-124Subventions
Organisme : Janssen Research and Development
ID : VX-950HHC001
Informations de copyright
© 2021 British Society for Immunology.
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