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The Journal of Immunology, 2001, 167: 1877-1881.
Copyright © 2001 by The American Association of Immunologists

Cutting Edge

Cutting Edge: Induction of IFN-{gamma} Production but Not Cytotoxicity by the Killer Cell Ig-Like Receptor KIR2DL4 (CD158d) in Resting NK Cells

Sumati Rajagopalan1, Jacqueline Fu and Eric O. Long

Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852

Activated NK cells lyse tumor cells and virus-infected cells and produce IFN-{gamma} upon contact with sensitive target cells. The regulation of these effector responses in resting NK cells is not well understood. We now describe a receptor, KIR2DL4, that has the unique property of inducing IFN-{gamma} production, but not cytotoxicity, by resting NK cells in the absence of cytokines. In contrast, the NK cell-activation receptors CD16 and 2B4 induced cytotoxicity but not IFN-{gamma} production. The induction by KIR2DL4 of IFN-{gamma} production by resting NK cells was blocked by an inhibitor of the p38 mitogen-activated protein kinase signaling pathway, in contrast to the IL-2-induced IFN-{gamma} secretion that was sensitive to inhibition of the extracellular signal-regulated kinase mitogen-activated protein kinase pathway. These results reveal a functional dichotomy (cytokine production vs cytotoxicity) in the response of resting NK cells, as dictated by the signals of individual receptors.




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