TLRs induce glycolytic metabolism in DCs through the PI3K/Akt pathway. (A) Glycolytic rate of DCs stimulated with LPS in the presence of the indicated concentrations of the PI3K inhibitor LY294002. (B) Glycolytic rate after LPS stimulation in akt1^+/+ and akt1^−/− DCs. The fold change in glycolytic rate was calculated relative to the untreated control for each genotype. (C) Glycolytic rate of DCs transduced with the retroviral vectors MIG (control) or MIG–active form of Akt (myr-Akt). The data represent the fold increase in glycolytic rate relative to unstimulated MIG-transduced DCs. (D) Rate of mitochondrial fatty acid β-oxidation in DCs cultured for 18 hours in medium alone (-) or after stimulation with LPS in the presence or absence of the PI3K inhibitor LY294002. (E) Rate of mitochondrial fatty acid β-oxidation in wild-type (akt1^+/+) or Akt-deficient (akt1^−/−) DCs cultured for 18 hours in medium alone (-) or after stimulation with LPS. (F) Rate of mitochondrial fatty acid β-oxidation in DCs transduced with empty vector (MIG) or expressing myr-Akt. Bars represent mean value of replicates. Error bars represent SDs. All data are representative of 2 or more independent experiments.