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The mechanistic basis for MC activation in this disorder is unknown. We now demonstrate that patients with AERD have markedly increased epithelial expression of the alarmin-like cytokine IL-33 in nasal polyps, as compared with polyps from aspirin-tolerant control subjects. The murine model of AERD, generated by dust mite priming of mice lacking microsomal PGE2 synthase (ptges\u2212\/\u2212 mice), shows a similar upregulation of IL-33 protein in the airway epithelium, along with marked eosinophilic bronchovascular inflammation. Deletion of leukotriene C4 synthase, the terminal enzyme needed to generate cysLTs, eliminates the increased IL-33 content of the ptges\u2212\/\u2212 lungs and sharply reduces pulmonary eosinophilia and basal secretion of MC products. Challenges of dust mite\u2013primed ptges\u2212\/\u2212 mice with lysine aspirin induce IL-33\u2013dependent MC activation and bronchoconstriction. Thus, IL-33 is a component of a cysLT-driven innate type 2 immune response that drives pathogenic MC activation and contributes substantially to AERD pathogenesis.<\/jats:p>","DOI":"10.4049\/jimmunol.1500905","type":"journal-article","created":{"date-parts":[[2015,9,4]],"date-time":"2015-09-04T22:28:47Z","timestamp":1441405727000},"page":"3537-3545","source":"Crossref","is-referenced-by-count":118,"title":["Aspirin-Exacerbated Respiratory Disease Involves a Cysteinyl Leukotriene\u2013Driven IL-33\u2013Mediated Mast Cell Activation Pathway"],"prefix":"10.1093","volume":"195","author":[{"given":"Tao","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Medicine, Harvard Medical School , Boston, MA 02115"},{"name":"Division of Rheumatology, Immunology and Allergy, Brigham and Women\u2019s Hospital , Boston, MA 02115"},{"name":"Jeff and Penny Vinik Center for Allergic Disease Research , Boston, MA 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