FATEMEH MARDANİ VALANDANİ, SADEGH GHORBANİ-DALİNİ, MANİ RAMZİ, HEYDAR AGHABABA, MEYSAM SARSHAR, NAJMEH HAGHGOO, NEGAR AZARPİRA
Experimental and Clinical Transplantation - 2021;19(8):849-855
Objectives: HLA-E is located on the nonclassical major histocompatibility complex class I and acts as the ligand for natural killer cells. Consequently, it has a main role in the regulation of innate immune responses by involving cell identification by natural killer cells. Differences in expression levels among HLA-E alleles have been suggested to affect transplant outcomes. In this study, we evaluated the effects of different HLA-E genotypes on allogeneic hema - topoietic stem cell transplant in southern Iran. Materials and Methods: We investigated 200 patients (donors and recipients) who underwent allogeneic hematopoietic stem-cell transplant and 100 normal participants (control group) in a case-control study. Detection of HLA-E polymorphisms was performed using a sequence-specific primer polymerase chain reaction method. Results: Statistical analyses indicated that genotypes in the transplant group were not distributed in accordance with Hardy-Weinberg equilibrium (χ 2 = 76.56; P < .001), whereas genotypes in the control group were distributed in accordance with Hardy- Weinberg equilibrium (χ 2 = 0.39; P = .53). No significant differences were observed in cumulative incidence of acute (P = .76; hazard ratio = 0.80; 95% confidence interval, 0.19-3.31) and chronic (P = .75, hazard ratio = 0.048; 95% confidence interval, 0.00) graft-versus-host disease in recipients harboring HLA-E*0103 allele compared with those homozygous for the HLA-E*0101 allele. The HLA-E*0103 allele showed a trend toward lower cumulative incidence of relapse compared with the homozygous HLA-E*0101 genotype (8% vs 21.5%; P = .37; hazard ratio = 2.50; 95% confidence interval, 0.32-19.20). Conclusions: Genotypes of the HLA-E molecule did not correlate with acute and chronic graft-versus-host disease in hematopoietic stem cell transplant recipients except for the HLA-E*0101*/*0103 genotype, which was protective in survival of our study patients.
