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Dendritic cells (DCs) increase their metabolic dependence on glucose and glycolysis to support their maturation, activation-related cytokine manufacturing, and T-cell stimulatory capacity. We’ve previously proven that this improve in glucose metabolism might be initiated by both Toll-like receptor (TLR) and C-kind lectin receptor (CLR) agonists. In addition, we’ve proven that the TLR-dependent demand for glucose is partially happy by intracellular glycogen shops. However, the function of glycogen metabolism in supporting CLR-dependent DC glycolytic demand has not been formally demonstrated. On this work, we have now 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 family, pyrin area-containing-three (NLRP3) inflammasome in response to each TLR- and CLR-mediated activation. These data help a model by which totally different courses of innate immune receptors functionally converge in their requirement for glycogen-dependent glycolysis to metabolically assist early DC activation. These research present new perception into how DC immune effector operate is metabolically regulated in response to diverse inflammatory stimuli.

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