An IFN-γ-Dependent Pathway Controls Stimulation of Memory Phenotype CD8+ T Cell Turnover In Vivo by IL-12, IL-18, and IFN-γ

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Abstract
Unlike naive T cells, memory phenotype (CD44high) 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 CD44high CD8+ stimulation in vivo. This pathway is IFN-γ rather than IFN-I dependent and is mediated by at least three cytokines, IL-12, IL-18, and IFN-γ. 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.