Year: 2008
Type: article
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.
Source: The Journal of Immunology
Institutions: Centre National de la Recherche Scientifique, Inserm, Centre d’Immunologie de Marseille-Luminy, Brown University, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Université d'Orléans, Scripps Research Institute, Assistance Publique Hôpitaux de Marseille, Hôpital de la Conception
Language: English
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: bronze
Awards: G275612811, G6990905296, G8761244087
OpenAlex ID: W1899804292