A significant effect of the KIR ligand HLA-C on fibrosis progression in chronic C hepatitis with or without liver transplantation.
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BORIS DOI
Date of Publication
December 30, 2015
Publication Type
Article
Division/Institute
Author
Buhler, Stéphane | |
Giostra, Emiliano | |
Gbame, Corinne | |
de Rham, Casimir | |
Mullhaupt, Beat | |
Majno, Pietro | |
Negro, Francesco | |
Bochud, Pierre-Yves | |
Villard, Jean |
Subject(s)
Series
Liver international
ISSN or ISBN (if monograph)
1478-3223
Publisher
Blackwell Munksgaard
Language
English
Publisher DOI
PubMed ID
26717049
Uncontrolled Keywords
Description
BACKGROUND & AIMS
The interaction of KIR with their HLA ligands drives the activation and inhibition of natural killer (NK) cells. NK cells could be implicated in the development of liver fibrosis in chronic hepatitis C.
METHODS
We analysed 206 non-transplanted and 53 liver transplanted patients, selected according to their Metavir fibrosis stage. Several variables such as the number of activator KIR or the HLA ligands were considered in multinomial and logistic regression models. Possible confounding variables were also investigated.
RESULTS
The KIRs were not significant predictors of the fibrosis stage. Conversely, a significant reduction of the HLA-C1C2 genotype was observed in the most advanced fibrosis stage group (F4) in both cohorts. Furthermore, the progression rate of fibrosis was almost 10 times faster in the subgroup of patients after liver transplantation and HLA-C1C2 was significantly reduced in this cohort compared to non-transplanted patients.
CONCLUSION
This study suggests a possible role of KIR and their ligands in the development of liver damage. The absence of C1 and C2 ligands heterozygosity could lead to less inhibition of NK cells and a quicker progression to a high level of fibrosis in patients infected by HCV, especially following liver transplantation. This article is protected by copyright. All rights reserved.
The interaction of KIR with their HLA ligands drives the activation and inhibition of natural killer (NK) cells. NK cells could be implicated in the development of liver fibrosis in chronic hepatitis C.
METHODS
We analysed 206 non-transplanted and 53 liver transplanted patients, selected according to their Metavir fibrosis stage. Several variables such as the number of activator KIR or the HLA ligands were considered in multinomial and logistic regression models. Possible confounding variables were also investigated.
RESULTS
The KIRs were not significant predictors of the fibrosis stage. Conversely, a significant reduction of the HLA-C1C2 genotype was observed in the most advanced fibrosis stage group (F4) in both cohorts. Furthermore, the progression rate of fibrosis was almost 10 times faster in the subgroup of patients after liver transplantation and HLA-C1C2 was significantly reduced in this cohort compared to non-transplanted patients.
CONCLUSION
This study suggests a possible role of KIR and their ligands in the development of liver damage. The absence of C1 and C2 ligands heterozygosity could lead to less inhibition of NK cells and a quicker progression to a high level of fibrosis in patients infected by HCV, especially following liver transplantation. This article is protected by copyright. All rights reserved.
File(s)
| File | File Type | Format | Size | License | Publisher/Copright statement | Content | |
|---|---|---|---|---|---|---|---|
| A significant effect of the KIR ligand HLA-C on fibrosis progression in chronic C hepatitis with or without liver transplantation..pdf | text | Adobe PDF | 257.04 KB | publisher | published |