Allergen Uptake, Activation, and IL-23 Production by Pulmonary Myeloid DCs Drives Airway Hyperresponsiveness in Asthma-Susceptible Mice 英文参考文献.docVIP

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Allergen Uptake, Activation, and IL-23 Production by Pulmonary Myeloid DCs Drives Airway Hyperresponsiveness in Asthma-Susceptible Mice 英文参考文献.doc

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Allergen Uptake, Activation, and IL-23 Production by Pulmonary Myeloid DCs Drives Airway Hyperresponsiveness in Asthma-Susceptible Mice 英文参考文献

AllergenUptake,Activation,andIL-23Productionby PulmonaryMyeloidDCsDrivesAirway HyperresponsivenessinAsthma-SusceptibleMice IanP.Lewkowich1,StephaneLajoie1,JenniferR.Clark1,NancyS.Herman1,AlyssaA.Sproles1 ,Marsha Wills-Karp1,2 * 1Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America, 2DepartmentofPediatrics,UniversityofCincinnatiCollegeofMedicine,Cincinnati,Ohio,UnitedStatesofAmerica Abstract Maladaptive,Th2-polarizedinflammatoryresponsesareintegraltothepathogenesisofallergicasthma.AsregulatorsofT cell activation, dendritic cells (DCs) are important mediators of allergic asthma, yet the precise signals which render endogenousDCs‘‘pro-asthmatic’’,andtheextenttowhichthesesignalsareregulatedbythepulmonaryenvironmentand host genetics, remains unclear. Comparative phenotypic and functional analysis of pulmonary DC populations in mice susceptible(A/J),orresistant(C3H)toexperimentalasthma,revealedthatsusceptibilitytoairwayhyperresponsivenessis associated with preferential myeloid DC (mDC) allergen uptake, and production of Th17-skewing cytokines (IL-6, IL-23), whereas resistance is associated with increased allergen uptake by plasmacytoid DCs. Surprisingly, adoptive transfer of syngeneic HDM-pulsed bone marrow derived mDCs (BMDCs) to the lungs of C3H mice markedly enhanced lung IL-17A production, and rendered them susceptible to allergen-driven airway hyperresponsiveness. Characterization of these BMDCsrevealedlevelsofantigenuptake,andTh17promotingcytokineproductionsimilartothatobservedinpulmonary mDCsfromsusceptibleA/Jmice.Collectivelythesedatademonstratethatthelungenvironmentpresentinasthma-resistant micepromotesrobustpDCallergenuptake,activation,andlimitsTh17-skewingcytokineproductionresponsiblefordriving pathologicTcellresponsescentraltothedevelopmentofallergen-inducedairwayhyperresponsiveness. Citation:LewkowichIP,LajoieS,ClarkJR,HermanNS,SprolesAA,etal.(2008)