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• W1909824557 endingPage "6011" @default.
• W1909824557 startingPage "6007" @default.
• W1909824557 abstract "Unlike naive T cells, memory phenotype (CD44(high)) T cells exhibit a high background rate of turnover in vivo. Previous studies showed that the turnover of memory phenotype CD8(+) (but not CD4(+)) cells in vivo can be considerably enhanced by products of infectious agents such as LPS. Such stimulation is TCR independent and hinges on the release of type I IFNs (IFN-I) which leads to the production of an effector cytokine, probably IL-15. In this study, we describe a second pathway of CD44(high) CD8(+) stimulation in vivo. This pathway is IFN-gamma rather than IFN-I dependent and is mediated by at least three cytokines, IL-12, IL-18, and IFN-gamma. As for IFN-I, these three cytokines are nonstimulatory for purified T cells and under in vivo conditions probably act via production of IL-15." @default.
• W1909824557 created "2016-06-24" @default.
• W1909824557 creator A5008199212 @default.
• W1909824557 creator A5029672643 @default.
• W1909824557 creator A5050054747 @default.
• W1909824557 date "2001-05-15" @default.
• W1909824557 modified "2023-09-23" @default.
• W1909824557 title "An IFN-γ-Dependent Pathway Controls Stimulation of Memory Phenotype CD8+ T Cell Turnover In Vivo by IL-12, IL-18, and IFN-γ" @default.
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• W1909824557 doi "https://doi.org/10.4049/jimmunol.166.10.6007" @default.
• W1909824557 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11342616" @default.
• W1909824557 hasPublicationYear "2001" @default.
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