commit f66b98fef015b38ff3910eeb167a4a63ee2d4162 Author: mathew18x31447 Date: Sat Jul 26 03:51:17 2025 +0800 Add 'On This Work' diff --git a/On-This-Work.md b/On-This-Work.md new file mode 100644 index 0000000..36b3581 --- /dev/null +++ b/On-This-Work.md @@ -0,0 +1 @@ +
Dendritic cells (DCs) improve their metabolic dependence on glucose and glycolysis to assist their maturation, activation-associated cytokine manufacturing, and T-cell stimulatory capability. We've previously shown that this increase in glucose metabolism might be initiated by both Toll-like receptor (TLR) and C-type lectin receptor (CLR) agonists. In addition, now we have 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. On this work, we've shown that DCs activated with fungal-associated β-glucan ligands exhibit acute glycolysis induction that is dependent on glycogen metabolism. Furthermore, [natural glycogen stabilizer](http://aiot7.com:3000/tomokovalazque) metabolism supports DC maturation, inflammatory cytokine manufacturing, and priming of the nucleotide-binding domain, leucine-wealthy-containing family, pyrin area-containing-3 (NLRP3) inflammasome in response to both TLR- and CLR-mediated activation. These knowledge help a model wherein different courses of innate immune receptors functionally converge of their requirement for glycogen-dependent glycolysis to metabolically support early DC activation. These studies provide new insight into how DC immune effector perform is metabolically regulated in response to diverse inflammatory stimuli.

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