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  TLR-driven early glycolytic reprogramming via the kinases TBK1-IKKɛ supports the anabolic demands of dendritic cell activation

Everts, B., Amiel, E., Huang, S.-C.-C., Smith, A. M., Chang, C.-H., Lam, W. Y., et al. (2014). TLR-driven early glycolytic reprogramming via the kinases TBK1-IKKɛ supports the anabolic demands of dendritic cell activation. Nature Immunology, 15, 323-332. doi:10.1038/ni.2833.

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Item Permalink: https://hdl.handle.net/21.11116/0000-0006-5432-3 Version Permalink: https://hdl.handle.net/21.11116/0000-0006-62D8-8
Genre: Journal Article

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 Creators:
Everts, Bart1, Author
Amiel, Eyal1, Author
Huang, Stanley Ching-Cheng1, Author
Smith, Amber M1, Author
Chang, Chih-Hao1, Author
Lam, Wing Y1, Author
Redmann, Veronika1, Author
Freitas, Tori C1, Author
Blagih, Julianna1, Author
van der Windt, Gerritje J W1, Author
Artyomov, Maxim N1, Author
Jones, Russell G1, Author
Pearce, Erika L.2, Author           
Pearce, Edward J.2, Author           
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1External Organizations, ou_persistent22              
2Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243648              

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 Abstract: The ligation of Toll-like receptors (TLRs) leads to rapid activation of dendritic cells (DCs). However, the metabolic requirements that support this process remain poorly defined. We found that DC glycolytic flux increased within minutes of exposure to TLR agonists and that this served an essential role in supporting the de novo synthesis of fatty acids for the expansion of the endoplasmic reticulum and Golgi required for the production and secretion of proteins that are integral to DC activation. Signaling via the kinases TBK1, IKKɛ and Akt was essential for the TLR-induced increase in glycolysis by promoting the association of the glycolytic enzyme HK-II with mitochondria. In summary, we identified the rapid induction of glycolysis as an integral component of TLR signaling that is essential for the anabolic demands of the activation and function of DCs.

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Language(s): eng - English
 Dates: 2014-04
 Publication Status: Issued
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 Rev. Type: Peer
 Identifiers: DOI: 10.1038/ni.2833
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Title: Nature Immunology
  Other : Nat. Immunol.
Source Genre: Journal
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Publ. Info: New York, NY : Nature America Inc.
Pages: - Volume / Issue: 15 Sequence Number: - Start / End Page: 323 - 332 Identifier: ISSN: 1529-2908
CoNE: https://pure.mpg.de/cone/journals/resource/974392607073