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Journal Article

c-Myc-induced transcription factor AP4 is requeired for host protection mediated by CD8+ T Cells

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Jonathen,  Curtis
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons201431

Pearce,  Erika L.
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Chou, C., Pinto, A. K., Jonathen, C., Persaud, S. P., Cella, M., Lin, C.-C., et al. (2014). c-Myc-induced transcription factor AP4 is requeired for host protection mediated by CD8+ T Cells. Nature Immunology, 15, 884-893.


Cite as: https://hdl.handle.net/21.11116/0000-0006-5425-2
Abstract
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.