|
|
||||||||
Published online before print February 13, 2008
| ||||||||||||||||||||||||||||||||||||||||||||||||||||
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 Peyers 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
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |