title: TCDD-Induced Activation of Aryl Hydrocarbon Receptor Inhibits Th17 Polarization and Regulates Non-Eosinophilic Airway Inflammation in Asthma.
abstract: The aryl hydrocarbon receptor (AhR), a transcription factor of the bHLH/PAS family, has recently been demonstrated to regulate T cell differentiation. Whether AhR activation participates in allergic airway inflammation remains unknown. In the current study, using a non-eosinophilic asthma model, we demonstrate that 2, 3, 7, 8-tetrachlorodibenzo-P-dioxin (TCDD), a potent AhR ligand, reduced the airway infiltration of neutrophils, airway hyperresponsiveness and Th17 cytokine expression. Furthermore, stimulation with TCDD promoted Treg differentiation and inhibited Th17 differentiation. However, the maturation of dendritic cells may not be inhibited by AhR activation. This study thus indicates a critical role of TCDD-induced AhR activation in the regulation of non-eosinophilic airway inflammation.
authors.affiliation: Department of Respiratory Medicine, Xinhua Hospital, Shanghai Jiao Tong, University School of Medicine, Shanghai 200092, China.
authors.forename: Xiao-ming
authors.initials: XM
authors.lastname: Li
authors.affiliation: Department of Respiratory Medicine, Xinhua Hospital, Shanghai Jiao Tong, University School of Medicine, Shanghai 200092, China.
authors.forename: Juan
authors.initials: J
authors.lastname: Peng
authors.affiliation: Department of Respiratory Medicine, Xinhua Hospital, Shanghai Jiao Tong, University School of Medicine, Shanghai 200092, China.
authors.forename: Wen
authors.initials: W
authors.lastname: Gu
authors.affiliation: Department of Respiratory Medicine, Xinhua Hospital, Shanghai Jiao Tong, University School of Medicine, Shanghai 200092, China.
authors.forename: Xue-jun
authors.initials: XJ
authors.lastname: Guo
mesh_terms: D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000235:genetics* / Q000276:immunology; D002454:Cell Differentiation / Q000235:genetics; D016764:Cell Polarity / Q000187:drug effects / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis; D003713:Dendritic Cells / Q000276:immunology / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D051379:Mice; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity; D018336:Receptors, Aryl Hydrocarbon / Q000235:genetics / Q000378:metabolism*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D058504:Th17 Cells / Q000187:drug effects* / Q000276:immunology
chemical_list: D016207:Cytokines; D000072317:Polychlorinated Dibenzodioxins; D018336:Receptors, Aryl Hydrocarbon