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J Leukoc Biol. 2019 Sep 11. doi: 10.1002/JLB.3A0819-207RR. [Epub ahead of print]

Syk-dependent glycolytic reprogramming in dendritic cells regulates IL-1β production to β-glucan ligands in a TLR-independent manner.

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Cellular, Molecular, and Biomedical (CMB) Sciences Graduate Program, University of Vermont, Burlington, Vermont, USA.
University of Vermont, Burlington, Vermont, USA.
Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, Vermont, USA.
Department of Biomedical and Health Sciences, University of Vermont, Burlington, Vermont, USA.


Dendritic cells (DCs) activated via TLR ligation experience metabolic reprogramming, in which the cells are heavily dependent on glucose and glycolysis for the synthesis of molecular building blocks essential for maturation, cytokine production, and the ability to stimulate T cells. Although the TLR-driven metabolic reprogramming events are well documented, fungal-mediated metabolic regulation via C-type lectin receptors such as Dectin-1 and Dectin-2 is not clearly understood. Here, we show that activation of DCs with fungal-associated β-glucan ligands induces acute glycolytic reprogramming that supports the production of IL-1β and its secretion subsequent to NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activation. This acute glycolytic induction in response to β-glucan ligands requires spleen tyrosine kinase signaling in a TLR-independent manner, suggesting now that different classes of innate immune receptors functionally induce conserved metabolic responses to support immune cell activation. These studies provide new insight into the complexities of metabolic regulation of DCs immune effector function regarding cellular activation associated with protection against fungal microbes.


NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3); dectin-1/2; dendritic cells (DCs); glycolysis; inflammasome; oxidative phosphorylation (OXPHOS); pattern recognition receptor (PRR); spleen tyrosine kinase (Syk); toll-like receptor (TLR)


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