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Glycogen Metabolism Supports Early Glycolytic Reprogramming and Activation in Dendritic Cells in Response to Both TLR and Syk-Dependent CLR Agonists

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Undergraduate student researcher or research employee, University of Vermont, Burlington, VT 05405, USA
2
Cellular, Molecular, and Biomedical Sciences Graduate Program, University of Vermont, Burlington, VT 05405, USA
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Department of Biomedical and Health Sciences, University of Vermont, Burlington, VT 05405, USA
*
Author to whom correspondence should be addressed.
Cells 2020, 9(3), 715; https://doi.org/10.3390/cells9030715
Received: 28 January 2020 / Revised: 9 March 2020 / Accepted: 11 March 2020 / Published: 14 March 2020
(This article belongs to the Special Issue Metabolic Reprogramming in Innate Immune Cell Fate and Function)
Dendritic cells (DCs) increase their metabolic dependence on glucose and glycolysis to support their maturation, activation-associated cytokine production, and T-cell stimulatory capacity. We have previously shown that this increase in glucose metabolism can be initiated by both Toll-like receptor (TLR) and C-type lectin receptor (CLR) agonists. In addition, we have shown that the TLR-dependent demand for glucose is partially satisfied by intracellular glycogen stores. However, the role of glycogen metabolism in supporting CLR-dependent DC glycolytic demand has not been formally demonstrated. In this work, we have shown that DCs activated with fungal-associated β-glucan ligands exhibit acute glycolysis induction that is dependent on glycogen metabolism. Furthermore, glycogen metabolism supports DC maturation, inflammatory cytokine production, and priming of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome in response to both TLR- and CLR-mediated activation. These data support a model in which different classes of innate immune receptors functionally converge in their requirement for glycogen-dependent glycolysis to metabolically support early DC activation. These studies provide new insight into how DC immune effector function is metabolically regulated in response to diverse inflammatory stimuli. View Full-Text
Keywords: glycolysis; glycogen; glucose; dendritic cells; metabolism; innate immunity glycolysis; glycogen; glucose; dendritic cells; metabolism; innate immunity
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Curtis, K.D.; Smith, P.R.; Despres, H.W.; Snyder, J.P.; Hogan, T.C.; Rodriguez, P.D.; Amiel, E. Glycogen Metabolism Supports Early Glycolytic Reprogramming and Activation in Dendritic Cells in Response to Both TLR and Syk-Dependent CLR Agonists. Cells 2020, 9, 715.

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