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NOX2-dependent immunosuppression in chronic myelomonocytic leukemia

Artikel i vetenskaplig tidskrift
Författare Johan Aurelius
Alexander Hallner
Olle Werlenius
Rebecca E Riise
L. Mollgard
M. Brune
M. Hansson
Anna Martner
Fredrik Bergh Thorén
Kristoffer Hellstrand
Publicerad i Journal of Leukocyte Biology
Volym 102
Nummer/häfte 2
Sidor 459-466
ISSN 0741-5400
Publiceringsår 2017
Publicerad vid Sahlgrenska Cancer Center
Sidor 459-466
Språk en
Länkar doi.org/10.1189/jlb.5VMA1116-454R
Ämnesord CMML, reactive oxygen species, NK cells, ROS, T cells, MDS/MPN, acute myeloid-leukemia, natural-killer-cells, reactive oxygen, metabolites, nk cells, histaminergic regulation, cytotoxic lymphocytes, oxidative stress, free survival, expression, apoptosis, Cell Biology, Hematology, Immunology, llin p, 1991, cell biochemistry and function, v9, p29
Ämneskategorier Cancer och onkologi

Sammanfattning

Chronic myelomonocytic leukemia (CMML) is a myeloproliferative and myelodysplastic neoplasm with few treatment options and dismal prognosis. The role of natural killer (NK) cells and other antileukemic lymphocytes in CMML is largely unknown. We aimed to provide insight into the mechanisms of immune evasion in CMML with a focus on immunosuppressive reactive oxygen species (ROS) formed by the myeloid cell NADPH oxidase-2 (NOX2). The dominant population of primary human CMML cells was found to express membrane-bound NOX2 and to release ROS, which, in turn, triggered extensive PARP-1-dependent cell death in cocultured NK cells, CD8(+) T effector memory cells, and CD8(+) T effector cells. Inhibitors of ROS formation and scavengers of extracellular ROS prevented CMML cell-induced lymphocyte death and facilitated NK cell degranulation toward Ab-coated, primary CMML cells. In patients with CMML, elevation of immature cell counts (CD34(+)) in blood was associated with reduced expression of several NK cell-activating receptors. We propose that CMML cells may use extracellular ROS as a targetable mechanism of immune escape.

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