http://purl.uniprot.org/citations/30647027 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/30647027 | http://www.w3.org/2000/01/rdf-schema#comment | "Natural killer (NK) cell function is regulated by inhibitory receptors, such as the family of killer immunoglobulin-like receptors (KIRs) and the NKG2A/CD94 heterodimer. These receptors recognize cognate HLA class I molecules on potential target cells, and recent studies imply that an HLA-B dimorphism at position -21 in the gene segment encoding the leader peptide dictates whether NK cell regulation primarily relies on the KIRs or the NKG2A/CD94 receptor. The impact of this HLA-B dimorphism on NK cell-mediated destruction of leukemic cells or on the course of leukemia is largely unknown. In a first part of this study, we compared functions of NK cells in subjects carrying HLA-B -21M or 21T using interleukin-2 (IL-2)-activated NK cells and leukemic cells from patients with acute myeloid leukemia (AML). Subjects carrying HLA-B -21M harbored better-educated NKG2A+ NK cells and displayed superior capacity to degranulate lytic granules against KIR ligand-matched primary leukemic blasts. Second, we aimed to define the potential impact of HLA-B -21 variation on the course of AML in a phase 4 trial in which patients received IL-2-based immunotherapy. In keeping with the hypothesis that 21M may be associated with improved NK cell functionality, we observed superior leukemia-free survival and overall survival in -21M patients than in -21T patients during IL-2-based immunotherapy. We propose that genetic variation at HLA-B -21 may determine the antileukemic efficacy of activated NK cells and the clinical benefit of NK cell-activating immunotherapy."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.org/dc/terms/identifier | "doi:10.1182/blood-2018-09-874990"xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/author | "Brune M."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/author | "Hussein B.A."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/author | "Hellstrand K."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/author | "Thoren F.B."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/author | "Aurelius J."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/author | "Martner A."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/author | "Ewald Sander F."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/author | "Hallner A."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/author | "Bernson E."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/date | "2019"xsd:gYear |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/name | "Blood"xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/pages | "1479-1488"xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/title | "The HLA-B -21 dimorphism impacts on NK cell education and clinical outcome of immunotherapy in acute myeloid leukemia."xsd:string |
http://purl.uniprot.org/citations/30647027 | http://purl.uniprot.org/core/volume | "133"xsd:string |
http://purl.uniprot.org/citations/30647027 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/30647027 |
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