Toll-like receptor-induced changes in glycolytic metabolism regulate dendritic cell activation.
By C. Krawczyk, T. Holowka, Jie Sun, J. Blagih, Eyal Amiel, Ralph J. Deberardinis, J. Cross, Euihye Jung, Craig B. Thompson, Russell G. Jones and 1 more. Blood, 2010
1,165 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/17675e0c48ecdf9e85de34578cdd81a632af2152
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In Immunology
- Erika L. Pearce
- Michael D. Buck
- Navdeep S. Chandel
- S. Kaech
- Luke A. O'Neill
- S. Weinberg
- Laura A. Sena
- Edward J. Pearce
Citations in the corpus
- Macrophage-mediated inflammation in metabolic disease (2011, background): “In mammals, innate immune cells (such as neutrophils, macrophages and dendritic cells) and adaptive immune cells (B and T cells) utilize high levels of glucose following activatio”
- Posttranscriptional control of T cell effector function by aerobic glycolysis. (2013, positive): “However, cells such as dendritic cells switch from OXPHOS to aerobic glycolysis upon TLR-induced activation but do not proliferate (Krawczyk et al., 2010).”
- Pyruvate Kinase M2 regulates Hif-1α activity and IL-1β induction, and is a critical determinant of the Warburg Effect in LPS-activated macrophages (2015, positive): “A uthor M anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript INTRODUCTION Insights into the critical role of metabolic reprogramming in host defense and inflammation have recently emerged (Krawczyk et al., 2010; O’Neill and Hardie, 2013).”
- Immunometabolism governs dendritic cell and macrophage function (2016, background): “DCs can also respond via specific GPCRs to the short chain fatty acid butyrate (Singh et al., 2014), which is a product of commensal bacteria, to adenosine/ATP (Li et al., 2012), and to lactic acid (Nasi et al., 2013).”
- Metabolic Regulation of Immune Responses (2014, background): “In fact, the suppression of β-oxidation of fatty acids and mitochondrial respiration in mature DCs was more pronounced than the increase in their glycolytic rate, the latter being mediated by the activation of PI3K-Akt pathway by the TLR ligands (78).”
- Regulation of glycolysis by the hypoxia‐inducible factor (HIF): implications for cellular physiology (2020, background): “A variety of immune cells, including dendritic cells (Krawczyk et al. 2010), classically activated M1 macrophages (Michl et al. 1976), neutrophils (Sbarra & Karnovsky, 1959), lymphocytes (T cells (Frauwirth et al. 2002; Wang et al. 2011) and B cells (Doughty et al. 2006)) adopt a high-glycolytic…”
- Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013, background): “TCR/CD28 stimulation of T cells (6), the stimulation of surface immunoglobulin on B cells (41), and TLR stimulation of macrophages and dendritic cells (DCs) (42, 43) all promote changes in aerobic glycolysis characteristic of the Warburg”
- Mitochondria in the regulation of innate and adaptive immunity (2015, positive): “The activation of this program using TLR stimulation results in a robust increase in glycolytic flux in dendritic cells (Everts et al., 2012; Krawczyk et al., 2010).”
- Microglial M1/M2 polarization and metabolic states (2016, background): “This switch increases glucose uptake and lactate production (Krawczyk et al., 2010; Rodríguez-Prados et al., 2010) with activation of the pentose phosphate pathway (PPP) and decreased mitochondrial oxygen consumption (Haschemi et al., 2012).”
- Metabolic Pathways In Immune Cell Activation And Quiescence (2013, background): “Moreover, there is evidence that inflamed tissues are deprived of oxygen, creating an environment where aerobic glycolysis is required for survival (Lewis et al., 1999).”