IL-33 is known to mediate its biological effects through ST2/IL1RL1[4] and sensitized mice with il1rl1 (ST2-/-) knocked out show less eosinophil numbers in bronchoalveolar lavage fluid upon allergen exposure than wild-type mice, reduced levels of Th2 cytokines and chemoattractants in the lungs, and reduced goblet cell hyperplasia around the peripheral airways in murine models of allergy and asthma[36, 37]. This evidence concerns the gene IL1RL1 and allergic disease.