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The Journal of Immunology, 2001, 166: 6007-6011.
Copyright © 2001 by The American Association of Immunologists

An IFN-{gamma}-Dependent Pathway Controls Stimulation of Memory Phenotype CD8+ T Cell Turnover In Vivo by IL-12, IL-18, and IFN-{gamma}1

David F. Tough2,*, Xiaohong Zhang{dagger} and Jonathan Sprent{dagger}

* Edward Jenner Institute for Vaccine Research, Compton, Newbury, Berkshire, United Kingdom; and {dagger} Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037

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-{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.




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