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Originally published online as doi:10.1189/jlb.0907626 on February 13, 2008

Published online before print February 13, 2008
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(Journal of Leukocyte Biology. 2008;83:1128-1135.)
© 2008 by Society for Leukocyte Biology

Characterization of a subset of bone marrow-derived natural killer cells that regulates T cell activation in rats

Taba Kheradmand1, Prachi P. Trivedi1,2, Norbert A. Wolf, Paul C. Roberts3 and Robert H. Swanborg4

Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, Michigan, USA

4Correspondence: Department of Immunology and Microbiology, Wayne State University School of Medicine, 540 East Canfield Ave., Detroit, MI 48201, USA. E-mail: rswanbo{at}med.wayne.edu

We report that bone marrow-derived natural killer (BMNK) cells from DA or F344 rats inhibit PMA/ionomycin-induced T cell proliferation. These NK-regulatory cells are NKR-P1Adim, whereas a minor subpopulation is NKR-P1Abright. Only the NKR-P1Adim BMNK cells inhibit T cell proliferation. If activated with rat Con A supernatant, the NKR-P1Adim cells become NKR-P1Abright and lose the ability to inhibit T cell proliferation. In contrast to BMNK cells, all DA and F344 rat NK cells isolated from the blood, spleen, cervical, or mesenteric lymph nodes or Peyer’s patches are NKR-P1Abright and lack the ability to inhibit T cell proliferation. Inhibition of T cell proliferation correlates with significant down-regulation of CD3, suggesting that this may be the mechanism through which the NKR-P1Adim cells mediate suppression. The nitric oxide synthase inhibitor NG-monomethyl-arginine acetate-abrogated NKR-P1Adim cell inhibition of T cell proliferation. We conclude that rat bone marrow NKR-P1Adim cells represent a unique population that may play a role in maintaining immune homeostasis by regulating the clonal expansion of activated T cells.

Key Words: suppression • tolerance • cytokines






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