2022
Innate and Adaptive Immunity to Transfused Allogeneic RBCs in Mice Requires MyD88.
Soldatenko A, Hoyt LR, Xu L, Calabro S, Lewis SM, Gallman AE, Hudson KE, Stowell SR, Luckey CJ, Zimring JC, Liu D, Santhanakrishnan M, Hendrickson JE, Eisenbarth SC. Innate and Adaptive Immunity to Transfused Allogeneic RBCs in Mice Requires MyD88. The Journal Of Immunology 2022, 208: 991-997. PMID: 35039331, PMCID: PMC10107373, DOI: 10.4049/jimmunol.2100784.Peer-Reviewed Original ResearchConceptsPattern recognition receptorsDendritic cellsDC activationAdaptive immunityClass of PRRsNon-ABO alloantibodiesRecipient dendritic cellsSplenic dendritic cellsMouse RBCsInflammatory cytokine responseTreatment of anemiaRBC transfusion therapyTransfused RBCsAlloantibody responsesAllogeneic RBCsSerious complicationsCytokine responsesTransfusion therapyRecognition receptorsMyD88TransfusionAlloimmunizationRBCsTRIFUnknown mechanism
2019
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
2016
Uricase Inhibits Nitrogen Dioxide–Promoted Allergic Sensitization to Inhaled Ovalbumin Independent of Uric Acid Catabolism
Ather JL, Burgess EJ, Hoyt LR, Randall MJ, Mandal MK, Matthews DE, Boyson JE, Poynter ME. Uricase Inhibits Nitrogen Dioxide–Promoted Allergic Sensitization to Inhaled Ovalbumin Independent of Uric Acid Catabolism. The Journal Of Immunology 2016, 197: 1720-1732. PMID: 27465529, PMCID: PMC4992621, DOI: 10.4049/jimmunol.1600336.Peer-Reviewed Original ResearchConceptsAllergic airway diseaseAllergic sensitizationAirway diseaseUric acidDevelopment of OVAOVA-specific responsesAirways of miceUric acid levelsAdaptive immune responsesOVA-specific AbT cell proliferationPowerful inhibitory effectEnvironmental air pollutantsImmune deviationOVA challengeOVA uptakeDendritic cellsCytokine productionAdjuvant activityImmune responseRespiratory diseaseMouse modelUric acid formationInhibitory effectAcid levels