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KIR/HLA‐I mismatching and risk of relapse in paediatric patients undergoing non‐haploidentical allogeneic haematopoietic stem cell transplantation
Author(s) -
Scquizzato Elisa,
Zambello Renato,
Teramo Antonella,
Baesso Ilenia,
Varotto Stefania,
Albergoni Maria Paola,
Boscaro Elisa,
Cesaro Simone,
Pillon Marta,
Calore Elisabetta,
Gazzola Maria Vittoria,
Semenzato Gianpietro,
Messina Chiara,
Trentin Livio
Publication year - 2011
Publication title -
pediatric transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 69
eISSN - 1399-3046
pISSN - 1397-3142
DOI - 10.1111/j.1399-3046.2010.01447.x
Subject(s) - human leukocyte antigen , medicine , genotype , transplantation , immunology , hematopoietic stem cell transplantation , haematopoiesis , stem cell , gene , genetics , biology , antigen
Scquizzato E, Zambello R, Teramo A, Baesso I, Varotto S, Albergoni MP, Boscaro E, Cesaro S, Pillon M, Calore E, Gazzola MV, Semenzato G, Messina C, Trentin L. KIR/HLA‐I mismatching and risk of relapse in paediatric patients undergoing non‐haploidentical allogeneic haematopoietic stem cell transplantation.
Pediatr Transplantation 2011: 15:198–204. © 2010 John Wiley & Sons A/S. Abstract: In HSCT setting, KIR‐driven alloreactivity might be better predicted if the donor KIR genotype is considered in addition to the recipient HLA genotype. The prediction of NK cell alloreactivity relies on the missing ligand in the recipient, a scenario that can be found in HLA‐identical and non‐identical allotransplants. The aim of this study was to investigate at genetic level the prognostic impact of recipient HLA‐I lacking for donor KIR on allotransplanted patients outcome. We analysed donors KIR genotype and HLA genotype of 60 paediatric patients who received related (n = 15) or unrelated (n = 45) transplantation. When patients were grouped based on the KIR gene type involved in the KIR/HLA‐I mismatch, we did not observe any relapse in the group of patients characterized by mismatches involving only inhibitory KIR. On the contrary, all relapses were observed in patients showing at least one activating gene involved in the mismatch (p < 0.05). Although the biological mechanism accounting for this putative genetic rule is still to be clarified, we suggest that a careful survey of KIR/HLA‐I mismatching should be taken into account in the selection of donor in related and unrelated HSCT.