Human leukocyte antigen-G 3' untranslated region polymorphisms are associated with better kidney allograft acceptance.

Autor: Cilião Alves DC; Program of Basic and Applied Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, São Paulo, Brazil. daianicristina@yahoo.com.br, de Oliveira Crispim JC, Castelli EC, Mendes-Junior CT, Deghaide NH, Barros Silva GE, Costa RS, Saber LT, Moreau P, Donadi EA
Jazyk: angličtina
Zdroj: Human immunology [Hum Immunol] 2012 Jan; Vol. 73 (1), pp. 52-9. Date of Electronic Publication: 2011 Oct 14.
DOI: 10.1016/j.humimm.2011.10.007
Abstrakt: Human leukocyte antigen-G (HLA-G) plays a well-recognized role in the modulation of the immune response, and HLA-G expression has been associated with increased graft survival and decreased rejection episodes. To investigate the role of the HLA-G 3' untranslated region (3'UTR) in renal transplantation, we evaluated several polymorphic sites (14-bp Del/Ins +3003T/C, +3010C/G, +3027C/A, +3035C/T, +3142G/C, and +3187A/G) in patients exhibiting or not exhibiting rejection episodes. A total of 104 patients (15 with acute and 48 with chronic rejection, and 41 with no rejection) and 142 healthy individuals were studied. HLA-G 3'UTR was typed by direct sequencing. The +3035C-C genotype was more frequent in patients exhibiting chronic rejection compared with healthy controls, and the +3035C-T genotype was less frequent in chronic rejection compared with patients without rejection (acute plus chronic) or compared with healthy controls. The +3187G-A genotype, in which the A allele is associated with increased mRNA degradation, showed increased frequency in the rejection group (acute plus chronic) when compared with healthy controls. The 14 base pair Deletion/Insertion genotype was marginally increased in patients with acute rejection. This is the first study to show associations among numerous polymorphic sites in the HLA-G 3'UTR in kidney allotransplantation, which may contribute to the understanding of HLA-G post-transcriptional mechanisms.
(Copyright © 2012 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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