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Originally published online as doi:10.1189/jlb.1103595 on March 23, 2004

Published online before print March 23, 2004
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(Journal of Leukocyte Biology. 2004;75:1111-1115.)
© 2004 by Society for Leukocyte Biology

Oxygen radical-induced natural killer cell dysfunction: role of myeloperoxidase and regulation by serotonin

Åsa Betten*,1, Claes Dahlgren{dagger}, Ulf-Henrik Mellqvist{ddagger}, Svante Hermodsson* and Kristoffer Hellstrand*

* Departments of Clinical Virology,
{dagger} Rheumatology and Inflammation Research, and
{ddagger} Hematology, Göteborg University, Sweden

1 Correspondence: Department of Virology, Göteborg University, Guldhedsgatan 10 B, S-413 46 Göteborg, Sweden. E-mail: Aasa.Betten{at}microbio.gu.se

Natural killer (NK) cells are functionally suppressed and induced to apoptosis by reactive oxygen species (ROS) produced by mononuclear phagocytes (MPs). These inhibitory events are reversed by the biogenic amine serotonin. MPs generate hydrogen peroxide (H2O2), which is processed further by myeloperoxidase (MPO) to even more toxic compounds. Earlier studies suggest that serotonin scavenges MP-derived oxygen radicals generated by the MPO-H2O2 system. These findings led us to explore the capability of MPO-deficient MPs to induce NK cell dysfunction. We show that MPs recovered from subjects with MPO deficiency trigger inhibition of NK cells. In addition, MPs recovered from healthy subjects conveyed suppression of NK cells in the presence of the MPO inhibitor ceruloplasmin. We conclude that ROS-dependent inhibition of NK cell function is unrestricted by the availability of MPO-derived oxygen radicals and that the protecting properties of serotonin may operate in the absence of functional MPO. Our data suggest a complex mechanism of MP-induced NK cell inhibition, which comprises the generation of interchangeable oxygen radicals.

Key Words: reactive oxygen species • NK cells • mononuclear phagocytes • MPO-deficient




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