Journal
NATURE IMMUNOLOGY
Volume 15, Issue 9, Pages 884-893Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2943
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Funding
- Lucille P. Markey Pathway Program
- Burroughs Wellcome Fund
- McDonnell International Scholars Academy at Washington University
- US National Institutes of Health [P30 AR048335, R01 AI097244, U54 AI081680]
- Edward Mallinckrodt Jr. Foundation
- Washington University Institute of Clinical and Translational Sciences of the National Center for Advancing Translational Sciences of the US National Institutes of Health [UL1 TR000448]
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Although the transcription factor c-Myc is essential for the establishment of a metabolically active and proliferative state in T cells after priming, its expression is transient. It remains unknown how T cell activation is maintained after c-Myc expression is downregulated. Here we identified AP4 as the transcription factor that was induced by c-Myc and sustained activation of antigen-specific CD8(+) T cells. Despite normal priming, AP4-deficient CD8(+) T cells failed to continue transcription of a broad range of c-Myc-dependent targets. Mice lacking AP4 specifically in CD8(+) T cells showed enhanced susceptibility to infection with West Nile virus. Genome-wide analysis suggested that many activation-induced genes encoding molecules involved in metabolism were shared targets of c-Myc and AP4. Thus, AP4 maintains c-Myc-initiated cellular activation programs in CD8(+) T cells to control microbial infection.
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