Innate partnership of HLA-B and KIR3DL1 subtypes against HIV-1
Détails
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_119EF928F3F4
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Innate partnership of HLA-B and KIR3DL1 subtypes against HIV-1
Périodique
Nature Genetics
ISSN
1061-4036 (Print)
Statut éditorial
Publié
Date de publication
06/2007
Peer-reviewed
Oui
Volume
39
Numéro
6
Pages
733-40
Langue
anglais
Notes
Journal Article
Multicenter Study
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't --- Old month value: Jun
Multicenter Study
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't --- Old month value: Jun
Résumé
Allotypes of the natural killer (NK) cell receptor KIR3DL1 vary in both NK cell expression patterns and inhibitory capacity upon binding to their ligands, HLA-B Bw4 molecules, present on target cells. Using a sample size of over 1,500 human immunodeficiency virus (HIV)+ individuals, we show that various distinct allelic combinations of the KIR3DL1 and HLA-B loci significantly and strongly influence both AIDS progression and plasma HIV RNA abundance in a consistent manner. These genetic data correlate very well with previously defined functional differences that distinguish KIR3DL1 allotypes. The various epistatic effects observed here for common, distinct KIR3DL1 and HLA-B Bw4 combinations are unprecedented with regard to any pair of genetic loci in human disease, and indicate that NK cells may have a critical role in the natural history of HIV infection.
Mots-clé
Alleles
Cohort Studies
Disease Progression
HIV Infections/genetics/*immunology/metabolism
HIV-1/*genetics
HLA-B Antigens/genetics/immunology/*metabolism
Humans
Immunity, Natural
Killer Cells, Natural/immunology
RNA, Viral/blood/genetics
Receptors, Immunologic/genetics/immunology/*metabolism
Viral Load
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/01/2008 15:46
Dernière modification de la notice
20/08/2019 13:39