Table of Contents Author Guidelines Submit a Manuscript
Journal of Immunology Research
Volume 2018, Article ID 3826989, 8 pages
Research Article

The Influence of Genetic Variations in the CD86 Gene on the Outcome after Allogeneic Hematopoietic Stem Cell Transplantation

1Department of Experimental Therapy, L. Hirszfeld Institute of Immunology & Experimental Therapy, Polish Academy of Sciences, R Weigl 12, 53-114 Wroclaw, Poland
2Urology and Urologic Oncology Department, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland
3Department of Hematology and Bone Marrow Transplantation, School of Medicine in Katowice, Medical University of Silesia, Dabrowskiego 25, 40-032 Katowice, Poland

Correspondence should be addressed to Lidia Karabon; lp.corw.nap.dtii@nobarakl

Received 23 August 2017; Accepted 14 November 2017; Published 7 February 2018

Academic Editor: Nejat K. Egilmez

Copyright © 2018 Lidia Karabon 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.


CD86 molecule is the ligand for both costimulatory (CD28) and coinhibitory (CTLA-4) molecules, and it regulates immune response after allogeneic hematopoietic stem cell transplantation (alloHSCT). Therefore, we postulate that CD86 gene variations might influence the outcome after alloHSCT. Altogether, 295 adult patients (pts) undergoing related (105 pts) and unrelated (190 pts) donor-matched HSCT were genotyped for the following CD86 gene polymorphisms: rs1129055, rs9831894, and rs2715267. Moreover, the donors’ rs1129055 polymorphism was determined. None of the investigated SNPs alone were associated with aGvHD and rate of relapse. However, we showed that rs2715267 SNP influenced overall survival (OS) after alloHSCT. The 24-month OS for the rs271526GG recipients was worse than that for the recipients possessing T allelle (TT or GT genotypes) (). Moreover, analysis of gene-gene interaction between CD86 and CTLA-4 showed that having both the A allele for CD86 rs1129055 and the CTLA-4 CT60GG genotype in recipients increased the risk of aGvHD about 3.5 times. Interestingly, the donors’ rs1129055GG genotype and the recipients’ CT60GG genotype also increased the risk of aGvHD about 2.7-fold. We postulate that recipients’ CD86 gene polymorphisms influence the overall survival after alloHSCT and, together with CTLA-4 polymorphisms, might be considered a risk factor for aGvHD.