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

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.