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Revision as of 06:00, 15 October 2025
Dendritic cells (DCs) increase their metabolic dependence on glucose and glycolysis to help their maturation, activation-associated cytokine production, and T-cell stimulatory capability. We've beforehand proven that this increase in glucose metabolism will be initiated by each Toll-like receptor (TLR) and C-type lectin receptor (CLR) agonists. In addition, we've got proven that the TLR-dependent demand for glucose is partially glad by intracellular glycogen stores. However, the position of glycogen metabolism in supporting CLR-dependent DC glycolytic demand has not been formally demonstrated. In this work, now we have shown that DCs activated with fungal-related 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 area, leucine-rich-containing household, pyrin domain-containing-three (NLRP3) inflammasome in response to each TLR- and CLR-mediated activation. These data assist a mannequin in which different lessons of innate immune receptors functionally converge in their requirement for glycogen-dependent glycolysis to metabolically assist early DC activation. These research provide new perception into how DC immune effector function is metabolically regulated in response to various inflammatory stimuli.
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