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Blood, 1 September 2000, Vol. 96, No. 5, pp. 1961-1968
PHAGOCYTES
Natural killer cell dysfunction and apoptosis induced by
chronic myelogenous leukemia cells: role of reactive oxygen species
and regulation by histamine
Ulf-Henrik Mellqvist,
Markus Hansson,
Mats Brune,
Claes Dahlgren,
Svante Hermodsson, and
Kristoffer Hellstrand
From the Hematology Section, Department of Medicine,
Institute of Medical Microbiology and Department of Virology,
Sahlgren's University Hospital, Göteborg, Sweden.
Natural killer (NK) cells are deficient in patients with chronic
myelogenous leukemia (CML), but the mechanisms responsible for the
dysfunction are not completely understood. This study reports that CML
cells effectively inhibit the baseline and interleukin-2 (IL-2)-induced
NK cell cytotoxicity against a CML cell-derived line (K562). A sizable
fraction of NK cells subsequently acquired features characteristic of
programmed cell death/apoptosis. The CML cell-mediated inhibition of NK
cells required triggering of reduced nicotinamide adenine dinucleotide
phosphate (NADPH) oxidase-mediated formation of reactive oxygen species
(ROS) and was prevented by catalase, a scavenger of ROS, and by
histamine, acting via H2-receptor-mediated inhibition of
ROS production in CML cells. In contrast, nonmalignant neutrophilic
granulocytes inhibited NK cells via ROS production without the
requirement of exogenous NADPH oxidase-triggering stimuli. We propose
that paracrine production of ROS may contribute to the dysfunction of
NK cells in CML and that histamine may serve as an autocrine inhibitor
of ROS formation in leukemic granulocytes.
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