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Dendritic cells (DCs) improve their metabolic dependence on glucose and glycolysis to support their maturation, activation-related cytokine manufacturing, and T-cell stimulatory capacity. We've got beforehand shown that this enhance in glucose metabolism may be initiated by each Toll-like receptor (TLR) and C-sort lectin receptor (CLR) agonists. In addition, we now have proven 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've got shown that DCs activated with fungal-related β-glucan ligands exhibit acute glycolysis induction that relies on glycogen metabolism. Furthermore, glycogen metabolism supports DC maturation, inflammatory cytokine production, and priming of the nucleotide-binding area, leucine-wealthy-containing household, pyrin area-containing-3 (NLRP3) inflammasome in response to each TLR- and CLR-mediated activation. These information assist a model during which different classes of innate immune receptors functionally converge of their requirement for glycogen-dependent glycolysis to metabolically support early DC activation. These studies provide new perception into how DC immune effector operate is metabolically regulated in response to various inflammatory stimuli.
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