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Characterization of a subset of bone marrow‐derived natural killer cells that regulates T cell activation in rats
Author(s) -
Kheradmand Taba,
Trivedi Prachi P.,
Wolf Norbert A.,
Roberts Paul C.,
Swanborg Robert H.
Publication year - 2008
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0907626
Subject(s) - biology , interleukin 21 , bone marrow , natural killer t cell , microbiology and biotechnology , interleukin 12 , mesenteric lymph nodes , cell growth , lymphokine activated killer cell , t cell , cell , immunology , population , immune system , cytotoxic t cell , in vitro , medicine , biochemistry , environmental health
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.