Table of Contents Author Guidelines Submit a Manuscript
Journal of Immunology Research
Volume 2016, Article ID 1910852, 8 pages
http://dx.doi.org/10.1155/2016/1910852
Clinical Study

HLA-01:03 Allele in Lung Transplant Recipients Correlates with Higher Chronic Lung Allograft Dysfunction Occurrence

1CNRS, EFS, ADES UMR 7268, Aix-Marseille Université, 13916 Marseille, France
2Immunogenetics Laboratory, EFS-Alpes Méditerranée, 13005 Marseille, France
3Department of Public Health, EA 3279 Research Unit, Marseille University Hospital, Aix-Marseille University, Marseille, France
4Service de Pneumologie, Hôpital Nord, 13015 Marseille, France
5Service de Chirurgie Thoracique, Hôpital Nord, 13015 Marseille, France

Received 30 March 2016; Revised 8 May 2016; Accepted 19 May 2016

Academic Editor: Fabio Morandi

Copyright © 2016 Julie Di Cristofaro et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Lung transplantation (LTx) is a valid therapeutic option for selected patients with end-stage lung disease. HLA-E seems to play a major role in the immune response to different viral infections and to affect transplantation outcome, in Hematopoietic Stem Cell Transplantation, for example. Two nonsynonymous alleles, HLA-01:01 and HLA-01:03, have functional differences, involving relative peptide affinity, cell surface expression, and potential lytic activity of NK cells. The aim of this retrospective study was to determine the impact of these two alleles for LTx recipients on anti-HLA alloimmunization risk, overall survival, and chronic rejection (CLAD). HLA-E was genotyped in 119 recipients who underwent LTx from 1998 to 2010 in a single transplantation center. In univariate analysis, both HLA-E homozygous states were associated with impaired overall survival compared to heterozygous HLA-E alleles (). In multivariate analysis, HLA-01:03 allele showed increased CLAD occurrence when compared to homozygous HLA-01:01 status (HR: 3.563 (CI 95%, 1.016–12), ). HLA-E allele did not affect pathogen infection or the production of de novo DSA. This retrospective study shows an uninvestigated, deleterious association of HLA-E alleles with LTx and requires verification using a larger cohort.