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Chronic myeloid leukemic cells trigger poly(ADP-ribose) polymerase-dependent inactivation and cell death in lymphocytes.

Journal article
Authors Johan Aurelius
Anna Martner
Rebecca E Riise
Ana Romero
Lars Palmqvist
Mats Brune
Kristoffer Hellstrand
Fredrik Bergh Thorén
Published in Journal of leukocyte biology
Volume 93
Issue 1
Pages 155-160
ISSN 1938-3673
Publication year 2013
Published at Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Institute of Medicine, Department of Internal Medicine and Clinical Nutrition
Institute of Biomedicine, Department of Infectious Medicine
Pages 155-160
Language en
Links dx.doi.org/10.1189/jlb.0512257
Subject categories Immunology in the medical area

Abstract

NK cells and T cells are commonly dysfunctional in CML, and their status may determine the course of disease. We aimed to define the molecular mechanisms of leukemia-induced immunosuppression with focus on the role of ROS and the PARP-1 pathway of cell death. Malignant granulocytes from patients with BCR-ABL-positive CML expressed the oxygen radical-producing enzyme NOX, produced large amounts of ROS, and triggered extensive cell death in NK cells. Inhibition of PARP-1 maintained NK cell viability in cocultures with suppressive leukemic cells. Under conditions of oxidative stress, PARP-1 inhibition upheld the capacity of NK cells to kill myeloid leukemic cells, in addition to restoring the proliferation and cytokine production of NK cells and cytotoxic T cells. Our findings are suggestive of a novel pathway of relevance to immunosuppression in CML.

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