Included in the MAP-kinase module was IL15 which has been inversely correlated with lung function in patients with severe asthma, and our finding that Th17 cells increased expression in the epithelium may provide a possible mechanism.22 The additive responses likely reflect the enhancement of an epithelial response in the setting of Th17 priming and highlight how epithelial-immune cell interplay can amplify an initial stimulus in the epithelium. Here, IL15 is linked to asthma.