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• W1899804292 startingPage "1627" @default.
• W1899804292 abstract "Abstract Recent evidence suggests that NK cells require priming to display full effector activity. In this study, we demonstrate that IL-18 contributed to this phenomenon. IL-18 signaling-deficient NK cells were found to be unable to secrete IFN-γ in response to ex vivo stimulation with IL-12. This was not due to a costimulatory role of IL-18, because blocking IL-18 signaling during the ex vivo stimulation with IL-12 did not alter IFN-γ production by wild-type NK cells. Rather, we demonstrate that IL-18 primes NK cells in vivo to produce IFN-γ upon subsequent stimulation with IL-12. Importantly, IL-12-induced IFN-γ transcription by NK cells was comparable in IL-18 signaling-deficient and -sufficient NK cells. This suggests that priming by IL-18 leads to an improved translation of IFN-γ mRNA. These results reveal a novel type of cooperation between IL-12 and IL-18 that requires the sequential action of these cytokines." @default.
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• W1899804292 date "2008-08-01" @default.
• W1899804292 modified "2023-10-16" @default.
• W1899804292 title "Cutting Edge: Priming of NK Cells by IL-18" @default.
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• W1899804292 doi "https://doi.org/10.4049/jimmunol.181.3.1627" @default.
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