In response to respiratory syncytial virus infection, epithelial cells from autophagy-deficient animals generated significant amounts of IL-1 and displayed accelerated IL-17-driven lung disease.162 The IL-17/IL-22 axis regulates homeostatic mechanisms, such as autophagy, and is critical in determining adverse outcomes to both viral and noninfectious inflammatory stimuli. Here, IL17A is linked to respiratory syncytial virus infectious disease.