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Published online before print February 13, 2008

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0907626

Received for publication September 12, 2007.
Revised January 11, 2008.
Accepted for publication January 17, 2008.

Article

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

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

^@ To whom correspondence should be addressed. E-mail: rswanbo{at}med.wayne.edu.

	Abstract

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-P1A^dim, whereas a minor subpopulation is NKR-P1A^bright. Only the NKR-P1A^dim BMNK cells inhibit T cell proliferation. If activated with rat Con A supernatant, the NKR-P1A^dim cells become NKR-P1A^bright 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-P1A^bright 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-P1A^dim cells mediate suppression. The nitric oxide synthase inhibitor N^G-monomethyl-arginine acetate-abrogated NKR-P1A^dim cell inhibition of T cell proliferation. We conclude that rat bone marrow NKR-P1A^dim 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