PT  - JOURNAL ARTICLE
AU  - Tough, David F.
AU  - Zhang, Xiaohong
AU  - Sprent, Jonathan
TI  - An IFN-γ-Dependent Pathway Controls Stimulation of Memory Phenotype CD8<sup>+</sup> T Cell Turnover In Vivo by IL-12, IL-18, and IFN-γ
AID  - 10.4049/jimmunol.166.10.6007
DP  - 2001 May 15
TA  - The Journal of Immunology
PG  - 6007--6011
VI  - 166
IP  - 10
4099  - http://www.jimmunol.org/content/166/10/6007.short
4100  - http://www.jimmunol.org/content/166/10/6007.full
SO  - J. Immunol.2001 May 15; 166
AB  - 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.