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Production and Cytotoxicity of IL-2-Activated Murine NK Cells Are Differentially Regulated by MHC Class I Molecules1
*
Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, Canada;
Unité de Biologie Moléculaire du Gène, Institut National de la Santé et de la Recherche Médicale Unit 277, Institute Pasteur, Paris, France; and
Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada
Activation of NK cells by target cells leads to cytotoxicity as
well as production of various cytokines including IFN-
. MHC class I
molecules on target cells regulate NK cytotoxicity. However, little is
known about the regulation of IFN- production by NK cells. We
examined the production of IFN- in individual murine NK cells
stimulated with tumor cell lines by flow cytometric analysis of
intracellular IFN-. Among several tumor lines tested, the rat
basophilic leukemia line RBL-1 induced particularly high level of
IFN- production in IL-2-activated NK cells, whereas other lines,
including the prototypic NK target YAC-1, induced very low or no
IFN- production. Transfection of murine classical MHC class I
molecules into RBL-1 cells substantially inhibited IFN- production.
This inhibition of IFN- production by MHC class I was independent of
Ly-49 or CD94/NKG2A expression on NK cells. These results indicate that
some target cells directly stimulate IL-2-activated NK cells and induce
IFN- production, but the requirements for the induction of IFN-
production seem different from those for NK cytotoxicity. Furthermore,
similar to NK cytotoxicity, induction of IFN- production is
inhibited by MHC class I on stimulating cells. However, the MHC class
I-specific receptors inhibiting IFN- production are different from
those for NK cytotoxicity.
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