The endogenous Th17 response in NO2-promoted allergic airway disease is dispensable for airway hyperresponsiveness and distinct from Th17 adoptive transfer.
Severe, glucocorticoid-resistant asthma comprises 5-7% of patients with asthma.IL-17 is a biomarker of severe asthma, and the adoptive transfer of Th17 cells in mice is sufficient to induce glucocorticoid-resistant allergic airway disease.Nitrogen dioxide (NO2) is an environmental toxin that correlates with asthma severity, exacerbation, and risk o