KIR2DL2/S2 and KIR2DS5 in alcoholic cirrhotic patients undergoing liver transplantation.
KIr genes
NK cells
alcohol
cirrhosis
human clinical toxicology
Journal
Archives of medical science : AMS
ISSN: 1734-1922
Titre abrégé: Arch Med Sci
Pays: Poland
ID NLM: 101258257
Informations de publication
Date de publication:
2021
2021
Historique:
received:
12
12
2018
accepted:
23
03
2019
entrez:
24
5
2021
pubmed:
9
4
2019
medline:
9
4
2019
Statut:
epublish
Résumé
The molecular mechanisms underlying alcoholic liver fibrosis and cirrhosis are not completely understood. Hepatic fibrosis involves the interplay of diverse cells and factors, including hepatic stellate cells (HSCs), Kupffer, NK cells, and T-lymphocyte subsets. Killer-cell immunoglobulin-like receptors (KIR) are membrane receptors involved in mediation between NK and activated HSCs, regulating NK cell function through their interaction with HLA-I molecules. The aim of this study was to analyse the genetic association between KIR genes and the susceptibility to or protection from alcoholic cirrhosis (AC) in a cohort of male AC patients undergoing liver transplantation (LT) with and without concomitant viral infections. KIR genotyping was performed in nuclear DNA extracted from 281 AC patients and compared with 319 male controls. Significant differences between total AC patients and healthy controls were only found in the case of KIR2DL2 and KIR2DS5. KIR2DL2 was significantly underrepresented in non-viral AC patients (52.6% vs. 63.3%; Our data suggest a contrary effect of KIR2DL2 and KIR2DS5 in AC patients older than 54 years, in whom the presence of KIR2DL2 appears to be protective against AC, whereas the presence of KIR2DS5 seems to promote the fibrotic process, particularly in patients with no associated viral infection.
Identifiants
pubmed: 34025847
doi: 10.5114/aoms.2019.84410
pii: 105908
pmc: PMC8130473
doi:
Types de publication
Journal Article
Langues
eng
Pagination
764-774Informations de copyright
Copyright: © 2019 Termedia & Banach.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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