When mice lacking IL-17A were epicutaneously co-sensitized with Ova and SEB, lung inflammation, particularly neutrophilic inflammation, to a less extent eosinophilic inflammation, and AHR were greatly attenuated, though not completely abolished, suggesting that topical SEB coexisting with allergen Ova can synergistically promotes Th17/IL-17 immunity that serves as a primary driver in causing lung inflammation and AHR. The gene discussed is IL17A; the disease is inflammatory response.