Cited by 1,064Immune Response and InflammationImmunotherapy and Immune ResponsesCancer, Hypoxia, and Metabolism

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

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Everts, Bart, Amiel, Eyal, Huang, Stanley Ching-Cheng, Smith, Amber M, Chang, Chih-Hao, Lam, Wing Y, Redmann, Veronika, Freitas, Tori C, Blagih, Julianna, van der Windt, Gerritje J W, Artyomov, Maxim N, Jones, Russell G, Pearce, Erika L, Pearce, Edward J·2014·Nature Immunology

DOI 10.1038/ni.2833PMC PMC4358322

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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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Authors: Everts, B., Amiel, E., Huang, S. C.-C., Smith, A. M., Chang, C.-H., Lam, W. Y., Redmann, V., Freitas, T. C., Blagih, J., van der Windt, G. J. W., Artyomov, M. N., Jones, R. G., Pearce, E. L., & Pearce, E. J.
Affiliations: Washington University in St. Louis (US)
University of Vermont (US)
Trudeau Institute (US)
McGill University (CA)
Corresponding author: Pearce, Erika L
Pearce, Edward J
ORCID: Everts, Bart
Amiel, Eyal
Huang, Stanley Ching-Cheng
Smith, Amber M
Chang, Chih-Hao
Blagih, Julianna
Artyomov, Maxim N
Jones, Russell G
Pearce, Erika L
Pearce, Edward J
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2014-02-23
Volume: 15
Issue: 4
Pages: 323-332
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.2833
PMC: PMC4358322
OpenAlex: W2054828149
Cited by: 1,064
References: 48
Citations by year: 2026: 75 · 2025: 84 · 2024: 89 · 2023: 99 · 2022: 93 · 2021: 119 · 2020: 127 · 2019: 97 · 2018: 81 · 2017: 72 · 2016: 61 · 2015: 44 · 2014: 21
FWCI: 30.13
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
Locations: Nature Immunology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Data Archiving and Networked Services (DANS) (submittedVersion)
Pure Amsterdam UMC (submittedVersion)
MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
Funders: Nederlandse Organisatie voor Wetenschappelijk Onderzoek
National Institutes of Health
National Cancer Institute (CA158823, CA164062, R21CA158823, R01CA164062)
National Institute of Allergy and Infectious Diseases (R01AI091965, AI049823, T32AI049823, R01AI053825, AI53825)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Keywords: dendritic cell activation, glycolytic reprogramming, Toll-like receptor signaling, TBK1, IKKε, Akt, hexokinase 2, fatty acid synthesis, mitochondrial association, endoplasmic reticulum expansion, Golgi apparatus, dendritic cell metabolism, oxidative phosphorylation
MeSH terms: Animals, Cell Differentiation, Cells, Cultured, Dendritic Cells, Fatty Acids, Glycolysis, Hexokinase, Lipopolysaccharides, Lymphocyte Activation, Mice, Inbred C57BL, Mice, Transgenic, T-Lymphocytes, Signal Transduction, Protein Serine-Threonine Kinases, Mice, Knockout, RNA, Small Interfering, Proto-Oncogene Proteins c-akt, Toll-Like Receptors, Mice, I-kappa B Kinase

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

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