Abstract：
: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.
journal_name
Celljournal_title
Cellauthors
Chang CH,Curtis JD,Maggi LB Jr,Faubert B,Villarino AV,O'Sullivan D,Huang SC,van der Windt GJ,Blagih J,Qiu J,Weber JD,Pearce EJ,Jones RG,Pearce ELdoi
10.1016/j.cell.2013.05.016subject
Has Abstractpub_date
2013-06-06 00:00:00pages
1239-51issue
6eissn
0092-8674issn
1097-4172pii
S0092-8674(13)00582-5journal_volume
153pub_type
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