Using CD11c-specific Atg5−/− mice the authors further showed that impaired autophagy in DCs resulted in increased IL-1 and IL-23 release, spontaneous AHR, severe neutrophilic and Th17 cell-mediated airway inflammation, and glucocorticoid resistance, while adoptive transfer of Atg5−/− CD11c+ DCs aggravated lung inflammation and increased IL-17 release in the allergic airways (Table 2, Figure S1). This evidence concerns the gene IL1B and inflammation.