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Dendritic cells (DCs) improve their metabolic dependence on glucose and glycolysis to support their maturation, activation-associated cytokine production, and Healthy Flow Blood T-cell stimulatory capability. We have now previously shown that this increase in glucose metabolism could be initiated by both Toll-like receptor (TLR) and C-sort lectin receptor (CLR) agonists. As well as, we have now proven that the TLR-dependent demand for glucose is partially happy by intracellular glycogen shops. However, the role of glycogen metabolism in supporting CLR-dependent DC glycolytic demand has not been formally demonstrated. On this work, we have proven that DCs activated with fungal-related β-glucan ligands exhibit acute glycolysis induction that is dependent on glycogen metabolism. Furthermore, glycogen metabolism helps DC maturation, boost blood flow naturally inflammatory cytokine manufacturing, and priming of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome in response to each TLR- and CLR-mediated activation. These data help a model by which completely different courses of innate immune receptors functionally converge of their requirement for glycogen-dependent glycolysis to metabolically help early DC activation. These studies provide new perception into how DC immune effector perform is metabolically regulated in response to diverse inflammatory stimuli.