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Cutting edge: Priming of NK cells by IL-18

Academic Article
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Overview

authors

  • Chaix, J.
  • Tessmer, M. S.
  • Hoebe, K.
  • Fuseri, N.
  • Ryffel, B.
  • Dalod, M.
  • Alexopoulou, L.
  • Beutler, Bruce
  • Brossay, L.
  • Vivier, E.
  • Walzer, T.

publication date

  • August 2008

journal

  • Journal of Immunology  Journal

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-gamma 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-gamma production by wild-type NK cells. Rather, we demonstrate that IL-18 primes NK cells in vivo to produce IFN-gamma upon subsequent stimulation with IL-12. Importantly, IL-12-induced IFN-gamma 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-gamma mRNA. These results reveal a novel type of cooperation between IL-12 and IL-18 that requires the sequential action of these cytokines.

subject areas

  • Animals
  • Cells, Cultured
  • Cross-Priming
  • Interferon-gamma
  • Interleukin-12
  • Interleukin-18
  • Killer Cells, Natural
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myeloid Differentiation Factor 88
  • Signal Transduction
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 18641298
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Additional Document Info

start page

  • 1627

end page

  • 1631

volume

  • 181

issue

  • 3

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