IL33 and asthma: Because mast cells are important sources of IL-13 and are in close proximity to the bronchial epithelium in asthma,110 it is noteworthy that IL-33–activated mast cells, as well as ILC2s, are able to drive a predominantly IL-13–regulated pattern of gene expression in normal human bronchial epithelial cells in vitro.111 Furthermore, ILC2s have been shown to directly impair epithelial barrier integrity through IL-13,112 whereas TH2 cells cause barrier leakiness through IL-4 and IL-13, an effect that can be prevented by inhibition of histone deacetylases.113