Journal
JOURNAL OF IMMUNOLOGY
Volume 179, Issue 2, Pages 1190-1197Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.179.2.1190
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Funding
- NIAID NIH HHS [AI-52351, AI-27028] Funding Source: Medline
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Studies in IFN-gamma-deficient mice suggest that the delivery of IFN-gamma to CD8(+) T cells early in virus infection programs their eventual contraction, thereby reducing the abundance of CD8(+) memory T cells. In this study, we show that such mice fail to completely eliminate virus infection and that, when evaluated without the confounding factor of persisting Ag, both CD4(+) and CD8(+) T cells undergo profound contraction when they are unable to receive IFN-gamma signals. Furthermore, the abundance of CD4(+) and CD8(+) memory cells that express the IFN-gamma receptor is similar to 100-fold higher than cells lacking this molecule. Thus, direct IFN-gamma signaling is not required for T cell contraction during virus infection, and it enhances, rather than suppresses, the development of virusspecific CD4(+) and CD8(+) T cell memory.
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