The 14-bp deletion in the HLA-G gene indicates a low risk for acute cellular rejection in heart transplant recipients
Background Human leukocyte antigen G (HLA-G) is a non-classical Ib molecule in the major histocompatibility complex. HLA-G has important immunosuppressive properties, and in the context of cardiac transplantation, is associated with a low risk of cellular rejection. A 14-bp insertion/deletion polymo...
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Veröffentlicht in: | The Journal of heart and lung transplantation 2011-07, Vol.30 (7), p.778-782 |
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Sprache: | eng |
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Zusammenfassung: | Background Human leukocyte antigen G (HLA-G) is a non-classical Ib molecule in the major histocompatibility complex. HLA-G has important immunosuppressive properties, and in the context of cardiac transplantation, is associated with a low risk of cellular rejection. A 14-bp insertion/deletion polymorphism in exon 8 of the HLA-G gene is associated with messenger RNA (mRNA) stability and expression of HLA-G. This study analyzed the relationship between HLA-G polymorphisms and serum HLA-G levels in patients after cardiac transplantation to determine if any specific HLA-G genotype is associated with cellular rejection. Methods Ninety-four heart transplant patients were genotyped for the 14-bp polymorphism. Serum HLA-G levels and cellular rejection grades were evaluated in all patients. Results The 14-bp polymorphism was significantly associated with serum HLA-G expression. Patients with the –14-bp/–14-bp genotype had significantly higher mean serum HLA-G levels (88.2 U/ml) than those patients with the +14-bp/–14-bp (52.8 U/ml) and +14-bp/+14-bp (32.2 U/ml) genotypes ( p = 0.004). The –14 bp/–14-bp genotype was significantly associated with fewer episodes of cellular rejection. Conclusions This study suggests that the 14-bp deletion in the HLA-G gene plays an important role in the expression of HLA-G and thus might be a clinically useful genetic indicator for cellular rejection risk after cardiac transplantation. |
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ISSN: | 1053-2498 1557-3117 |
DOI: | 10.1016/j.healun.2011.01.726 |