Syk-dependent glycolytic reprogramming in dendritic cells regulates IL-1β production to β-glucan ligands in a TLR-independent manner
Thwe PM, Fritz DI, Snyder JP, Smith PR, Curtis KD, O'Donnell A, Galasso NA, Sepaniac LA, Adamik BJ, Hoyt LR, Rodriguez PD, Hogan TC, Schmidt AF, Poynter ME, Amiel E. Syk-dependent glycolytic reprogramming in dendritic cells regulates IL-1β production to β-glucan ligands in a TLR-independent manner. Journal Of Leukocyte Biology 2019, 106: 1325-1335. PMID: 31509298, PMCID: PMC6883127, DOI: 10.1002/jlb.3a0819-207rr.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBeta-GlucansDendritic CellsGlycolysisInterleukin-1betaLectins, C-TypeLigandsMiceMyeloid Differentiation Factor 88NLR Family, Pyrin Domain-Containing 3 ProteinPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSignal TransductionSyk KinaseToll-Like ReceptorsConceptsTLR-independent mannerDendritic cellsGlucan ligandMetabolic regulationMetabolic reprogramming eventsGlycolytic reprogrammingPyrin domain-containing protein 3 (NLRP3) inflammasome activationActivation of DCsProtein 3 inflammasome activationC-type lectin receptorsImmune effector functionsReprogramming eventsIL-1β productionImmune cell activationInnate immune receptorsFungal microbesMetabolic reprogrammingTyrosine kinaseReprogrammingImmune receptorsCytokine productionIL-1βT cellsInflammasome activationEffector functions