Journal
NATURE IMMUNOLOGY
Volume 10, Issue 5, Pages 504-513Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1729
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Funding
- American Cancer Society
- Robert A. and Renee E. Belfer Institute for Innovative Cancer Research
- US National Cancer Institute
- Division of Biological Sciences of the University of California, San Diego
- Fondation pour la Recherche Medicale
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Foxo transcription factors regulate cell cycle progression, cell survival and DNA-repair pathways. Here we demonstrate that deficiency in Foxo3 resulted in greater expansion of T cell populations after viral infection. This exaggerated expansion was not T cell intrinsic. Instead, it was caused by the enhanced capacity of Foxo3-deficient dendritic cells to sustain T cell viability by producing more interleukin 6. Stimulation of dendritic cells mediated by the coinhibitory molecule CTLA-4 induced nuclear localization of Foxo3, which in turn inhibited the production of interleukin 6 and tumor necrosis factor. Thus, Foxo3 acts to constrain the production of key inflammatory cytokines by dendritic cells and to control T cell survival.
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