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• W2028348534 abstract "HLA-E is a nonclassical human leukocyte antigen (HLA) class I gene with two antithetical products HLA-E*0101 and HLA-E*0103. They are found on most tissues (1), HLA-E*0103 being expressed at considerably higher levels than HLA-E*0101. These differences depend on the affinity for available peptides and on the stability of refolded complexes (2). We correlated the HLA-E polymorphism with the outcome of hematopoietic stem-cell transplantation (HSCT) with unrelated donors. The median follow-up time of 124 patients transplanted at the University Hospital in Vienna between September 1995 and December 2005 was 80 months (range 35–158 months). Clinical endpoints were acute graft-versus-host disease (aGvHD) and chronic graft-versus-host disease (cGvHD), transplant-related mortality (TRM), relapse, and overall survival. Finally, 121 patients were evaluated for aGvHD and 102 for cGvHD. All patient donor pairs were matched for HLA-A, -B, -C, -DRB1, -DRB3/4/5, and -DQB1 alleles at four digit resolution. Patient and donor characteristics used in the statistical models are summarized in Table 1. Donor selection criteria, assessment of aGvHD and cGvHD, and supportive care during HSCT have been previously described (3). Statistical analyses comprised simple and multiple Cox regression models and competing risk analyses (4). HLA-E typing was performed by sequencing based typing of axon 3.TABLE 1: Patient and donor characteristics and transplantation variablesThe distribution of HLA-E alleles was similar in patients (HLA-E*0101: n=45, 37%; HLA-E*0101, *0103: n=53, 43%; HLA-E*0103: n=24, 20%) and donors (HLA-E*0101: n=38, 31%; HLA-E*0101, *0103: n=56, 46%; HLA-E*0103: n=28, 23%). Two patients and two donors could not be typed due to missing DNA samples. Simple and competing risk analyses did not show evidence of an association of either of the analyzed genetic factors with clinical endpoints. Multiple regression analyses, however, showed associations with aGvHD (II–IV) (cumulative incidence at 80 days 41%, 95% confidence interval [CI] 30–49), overall cGvHD (cumulative incidence at 3 years 39%, 95% CI 28–48), relapse (cumulative incidence at 3 years, 39% 95% CI 29–48), and TRM (cumulative incidence at 180 days 17%, 95% CI 10–23). As to GvHD, HLA-E*0103, *0103 in donors was associated with a decreased risk of aGvHD (II–IV) (hazards ratio [HR] 0.39, 95% CI 0.16–0.99, P=0.047), whereas HLA-E*0101, *0103 in donors was associated with a decreased risk of overall cGvHD (HR 0.36, 95% CI 0.14–0.90, P=0.030). Regarding relapse, HLA-E*0103 alleles were associated with a higher risk (HR 2.24, 95% CI 1.03–4.88, P=0.042). Concerning TRM, HLA-E*0103, *0103 in donors was a risk factor (HR 3.94, 95% CI 1.03–15.02, P=0.045), whereas the presence of HLA-E*0101 alleles was protective (HR 0.32, 95% CI 0.11–0.94, P=0.037). In summary, the presence of HLA-E*0103 in donors is associated with decreased risks of aGvHD (II–IV) and cGvHD and an increased risk of relapse. Regarding early posttransplant effects, HLA-E*0103 is associated with an increased risk of TRM. In addition to the genetic factors, multiple analyses showed significantly increased risk of TRM in patients with aGvHD (I–IV), in patients at high-risk disease stage at transplantation, and in patients with donors older than 27 years (data not shown). Tamouza et al. (5) were the first to describe an association of HLA-E polymorphism with TRM in HSCT with unrelated donors. In their study, however, they found an association of HLA-E*0101, *0101 with increased TRM. This discrepancy might be due to differences between study populations (Tamouza et al. included also pediatric patients) and clinical protocols used. Especially, patients with bone marrow failure syndromes were more frequent in the Tamouza et al. study (27% vs. 0.8% in our patients). Patients suffering from bone marrow failure syndromes have high mortality rates after unrelated donor HSCT (6). The source of stem cells represents another difference (7). Although in our study, 56.5% of patients received peripheral blood stem cells, all patients in the study of Tamouza et al. had been transplanted with bone marrow-derived cells, known to prolong the time to hematologic and immunologic reconstitution and, therefore, prolong susceptibility to infections. Even though HLA-E*0103 allele cell surface expression exceeds that of HLA-E*0101 (8), a similar correlation in the effectiveness of viral or bacterial antigen presentation has not been shown. Moreover, an impaired efficiency of HLA-E*0103 alleles in minor histocompatibility antigen presentation and T-lymphocyte stimulation has been postulated (9). Inefficient presentation of minor histocompatibility antigens by HLA-E*0103 would be consistent with less aGvHD, an increased relapse rate, and increased TRM due to infections, as observed in our patients. Although our donor selection was based on a 12 of 12 allelic match, 47% of the pairs were mismatched for HLA-E alleles indicating different haplotypes. Therefore, it is possible that HLA-E serves as a surrogate marker for adjacent polymorphic loci that confer the effects we have observed. Katarina Ludajic Agathe Rosenmayr Ingrid Faé Gottfried F. Fischer Division of Blood Group Serology Medical University of Vienna Vienna, Austria Yesilda Balavarca Heike Bickeböller Department of Genetic Epidemiology University of Goettingen Goettingen, Germany Peter Kalhs Hildegard T. Greinix Department of Internal Medicine I Bone Marrow Transplantation Medical University of Vienna Vienna, Austria" @default.
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• W2028348534 title "Association of HLA-E Polymorphism With the Outcome of Hematopoietic Stem-Cell Transplantation With Unrelated Donors" @default.
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