Posttranscriptional control of T cell effector function by aerobic glycolysis.
Cell
; 153(6): 1239-51, 2013 Jun 06.
Article
en En
| MEDLINE
| ID: mdl-23746840
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.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Fosforilación Oxidativa
/
Activación de Linfocitos
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Linfocitos T
/
Glucólisis
Límite:
Animals
Idioma:
En
Revista:
Cell
Año:
2013
Tipo del documento:
Article
País de afiliación:
Estados Unidos