Given our promising results in the acute model of Th17-dependent airway inflammation, we assessed the effects of rapamycin in a chronic airway inflammation model.Here the pulmonary inflammation after the second challenge (d18/d19) relies on endogenously generated IL-17-producing cells due to the first challenge (d2-3), as we could demonstrate using RORgt-reporter mice16 as acceptors (Fig. 1a,b). This evidence concerns the gene IL17A and inflammatory response.