Journal
IMMUNITY
Volume 35, Issue 6, Pages 871-882Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2011.09.021
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Funding
- St Jude Children Hospital
- Damon Runyon-Rachleff Innovator Award
- NIH [AI081773, S064599, AR053573, AI40646, GM52735]
- American Lebanese and Syrian Associated Charities
- Sass Foundation for Medical Research
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To fulfill the bioenergetic and biosynthetic demand of proliferation, T cells reprogram their metabolic pathways from fatty acid beta-oxidation and pyruvate oxidation via the TCA cycle to the glycolytic, pentose-phosphate, and glutaminolytic pathways. Two of the top-ranked candidate transcription factors potentially responsible for the activation-induced T cell metabolic transcriptome, HIF1 alpha and Myc, were induced upon T cell activation, but only the acute deletion of Myc markedly inhibited activation-induced glycolysis and glutaminolysis in T cells. Glutamine deprivation compromised activation-induced T cell growth and proliferation, and this was partially replaced by nucleotides and polyamines, implicating glutamine as an important source for biosynthetic precursors in active T cells. Metabolic tracer analysis revealed a Myc-dependent metabolic pathway linking glutaminolysis to the biosynthesis of polyamines. Therefore, a Myc-dependent global metabolic transcriptome drives metabolic reprogramming in activated, primary T lymphocytes. This may represent a general mechanism for metabolic reprogramming under patho-physiological conditions.
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