The Endogenous Th17 Response in NO2-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer
Martin RA, Ather JL, Daggett R, Hoyt L, Alcorn JF, Suratt BT, Weiss DJ, Lundblad LK, Poynter ME. The Endogenous Th17 Response in NO2-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer. PLOS ONE 2013, 8: e74730. PMID: 24069338, PMCID: PMC3778003, DOI: 10.1371/journal.pone.0074730.Peer-Reviewed Original ResearchConceptsAllergic airway diseaseAirway hyperresponsivenessAirway diseaseAdoptive transferAntigen challengeCytokine productionNeutrophil recruitmentIL-1RDevelopment of AHRIL-1 receptor signalingLung cellsGlucocorticoid-resistant asthmaIL-17A neutralizationOTII T cellsAdaptive immune responsesDecreased neutrophil recruitmentAHR developmentClinical asthmaMixed Th2Antigen restimulationSevere asthmaTh17 cellsIL-17Th17 responsesAsthma severity