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• W4313342465 endingPage "3647" @default.
• W4313342465 startingPage "3642" @default.
• W4313342465 abstract "Abstract We analyzed the molecular mechanisms by which IL-12 and IL-18 induce transcriptional activity of the IFN-γ promoter in primary human CD4+ T cells. In transfection experiments, we found that IL-18 directly induces IFN-γ promoter activity, whereas significant activation with IL-12 required costimulation with αCD3/CD28. Furthermore, IL-12 caused in vivo protection of a STAT4 (−236) binding site, whereas stimulation with IL-18 or IL-12 plus αCD3/CD28 induced occupancy of a downstream AP-1 site. Mutation of this AP-1 site abrogated both IL-12- and IL-18-mediated promoter activation, whereas mutation of the STAT site inhibited IL-12-dependent activation. These data suggest that both AP-1 and STAT4 are required for IL-12-dependent IFN-γ promoter activity, whereas IL-18 causes direct activation via AP-1. This differential activation of the IFN-γ promoter gives further insights into molecular pathways governing Th1 T cell development and differentiation." @default.
• W4313342465 created "2023-01-06" @default.
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• W4313342465 date "1998-04-15" @default.
• W4313342465 modified "2023-10-17" @default.
• W4313342465 title "Cutting Edge: IL-12 and IL-18 Differentially Regulate the Transcriptional Activity of the Human IFN-γ Promoter in Primary CD4+ T Lymphocytes" @default.
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• W4313342465 doi "https://doi.org/10.4049/jimmunol.160.8.3642" @default.
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