Toll-like receptor–induced changes in glycolytic metabolism regulate dendritic cell activation
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Abstract
Dendritic cells (DCs) are key regulators of innate and acquired immunity. The maturation of DCs is directed by signal transduction events downstream of toll-like receptors (TLRs) and other pattern recognition receptors. Here, we demonstrate that, in mouse DCs, TLR agonists stimulate a profound metabolic transition to aerobic glycolysis, similar to the Warburg metabolism displayed by cancer cells. This metabolic switch depends on the phosphatidyl inositol 3'-kinase/Akt pathway, is antagonized by the adenosine monophosphate (AMP)-activated protein kinase (AMPK), and is required for DC maturation. The metabolic switch induced by DC activation is antagonized by the antiinflammatory cytokine interleukin-10. Our data pinpoint TLR-mediated metabolic conversion as essential for DC maturation and function and reveal it as a potential target for intervention in the control of excessive inflammation and inappropriately regulated immune responses.
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The record
- Venue
- Blood
- Topic
- Immune cells in cancer
- Field
- Immunology and Microbiology
- Canadian institutions
- McGill UniversityOccupational Cancer Research Centre
- Funders
- National Cancer InstituteNational Institute of Allergy and Infectious DiseasesCanadian Institutes of Health ResearchNational Institutes of HealthCancer Research Institute
- Keywords
- Cell biologySignal transductionBiologyAMPKInflammationGlycolysisDendritic cellReceptorImmune systemCytokineKinaseProtein kinase AMetabolismImmunologyBiochemistry
- Has abstract in OpenAlex
- yes