XPosttranscriptional control of T cell effector function by aerobic glycolysis

Chih Hao Chang, Jonathan D. Curtis, Leonard B. Maggi, Brandon Faubert, Alejandro V. Villarino, David O'Sullivan, Stanley Ching Cheng Huang, Gerritje J.W. Van Der Windt, Julianna Blagih, Jing Qiu, Jason D. Weber, Edward J. Pearce, Russell G. Jones, Erika L. Pearce

Research output: Contribution to journalArticlepeer-review

1536 Scopus citations


A "switch" from oxidative phosphorylation (OXPHOS) to aerobic glycolysis is a hallmark of T cell activation and is thought to be required to meet the metabolic demands of proliferation. However, why proliferating cells adopt this less efficient metabolism, especially in an oxygen-replete environment, remains incompletely understood. We show here that aerobic glycolysis is specifically required for effector function in T cells but that this pathway is not necessary for proliferation or survival. When activated T cells are provided with costimulation and growth factors but are blocked from engaging glycolysis, their ability to produce IFN-γ is markedly compromised. This defect is translational and is regulated by the binding of the glycolysis enzyme GAPDH to AU-rich elements within the 3′ UTR of IFN-γ mRNA. GAPDH, by engaging/disengaging glycolysis and through fluctuations in its expression, controls effector cytokine production. Thus, aerobic glycolysis is a metabolically regulated signaling mechanism needed to control cellular function. PaperFlick

Original languageEnglish
Pages (from-to)1239
Number of pages1
Issue number6
StatePublished - Jun 6 2013


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