ArticleRedox biology2026
Aryl hydrocarbon receptor in club cells drives Th17-mediated lung injury following inhalation exposure to environmentally persistent free radicals.
Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Environmentally persistent free radicals (EPFRs), generated during thermal combustion processes including hazardous waste remediation, are emerging redox-active pollutants linked to adverse respiratory outcomes. EPFR inhalation induces neutrophilic asthma characterized by substantial lung injury. Neutrophilic asthma is driven by T helper 17 (Th17) cells which secrete IL-17. We identified aryl hydrocarbon receptor (AHR) as a key mediator of EPFR-induced pulmonary Th17 responses. Building on this, we discovered that club cells, specialized airway epithelial cells, are a primary site of AHR activation following EPFR exposure. To dissect the specific role of AHR in club cells, we generated mice with a conditional deletion of Ahr in club cells (AhrΔCC) by crossing Ahr
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