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The HLA-B-21 dimorphism impacts on NK cell education and clinical outcome of immunotherapy in acute myeloid leukemia

Artikel i vetenskaplig tidskrift
Författare Alexander Hallner
Elin Bernson
Brwa Ali Hussein
Frida Ewald Sander
Mats Brune
Johan Aurelius
Anna Martner
Kristoffer Hellstrand
Fredrik Bergh Thorén
Publicerad i Blood
Volym 133
Nummer/häfte 13
Sidor 1479-1488
ISSN 0006-4971
Publiceringsår 2019
Publicerad vid Sahlgrenska Cancer Center
Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor 1479-1488
Språk en
Länkar dx.doi.org/10.1182/blood-2018-09-87...
Ämnesord mhc class-i, natural-killer-cells, hla-c expression, inhibitory, receptors, activation, relapse, association, cd94/nkg2a, molecules, infection
Ämneskategorier Hematologi

Sammanfattning

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 -21Mor 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 NKG2A1 NK cells and displayed superior capacity to degranulate lytic granules against KIR ligandmatched 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-2based 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-2based 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.

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