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  Toll-like receptor-induced changes in glycolytic metabolism regulate dendritic cell activation

Krawczyk, C. M., Holowka, T., Sun, J., Blagih, J., Amiel, E., DeBerardinis, R. J., et al. (2010). Toll-like receptor-induced changes in glycolytic metabolism regulate dendritic cell activation. PLoS Pathogens, 6, e1000840. doi:10.1182/blood-2009-10-249540.

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Krawczyk et al..pdf (Publisher version), 421KB
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 Creators:
Krawczyk, Connie M.1, Author
Holowka, Thomas1, Author
Sun, Jie1, Author
Blagih, Julianna1, Author
Amiel, Eyal1, Author
DeBerardinis, Ralph J.1, Author
Cross, Justin R.1, Author
Jung, Euihye1, Author
Thompson, Craig B.1, Author
Jones, Russell G.1, Author
Pearce, Edward J.2, Author              
Affiliations:
1External Organizations, ou_persistent22              
2Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243648              

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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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Language(s): eng - English
 Dates: 2010
 Publication Status: Published in print
 Pages: -
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 Rev. Type: Peer
 Identifiers: DOI: 10.1182/blood-2009-10-249540
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Title: PLoS Pathogens
  Other : PLoS Pathog.
Source Genre: Journal
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Publ. Info: San Francisco, CA : Public Library of Science
Pages: - Volume / Issue: 6 Sequence Number: - Start / End Page: e1000840 Identifier: ISSN: 1553-7366
CoNE: https://pure.mpg.de/cone/journals/resource/1000000000018830