Using genetically modified animals, deficiency of IL-22 resulted in increased AHR, eosinophilic airway inflammation, goblet cell metaplaisa, accumulation of IL-4 and IL-5 producing cells in the lung as well as increased levels of IL-5, IL-13, CCL17 and CCL26 in BAL fluid and lung tissue compared to challenged only mice. The gene discussed is CCL17; the disease is inflammatory response.