• Male mice showed a trend toward greater susceptibility to EPFR-induced Th17 responses and airway hyperresponsiveness driven by club cell AHR, suggesting potential sex-specific effects in pollutant-induced lung injury. • This study reveals a novel epithelial-immune axis linking pollutant sensing to Th17-mediated lung injury.
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Aryl hydrocarbon receptor in club cells drives Th17-mediated lung injury following inhalation exposure to environmentally persistent free radicals.
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