{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T22:44:09Z","timestamp":1790376249538,"version":"4.1.0"},"reference-count":65,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2018,2,1]],"date-time":"2018-02-01T00:00:00Z","timestamp":1517443200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Cysteinyl leukotrienes (cysLTs) facilitate mucosal type 2 immunopathology by incompletely understood mechanisms. Aspirin-exacerbated respiratory disease, a severe asthma subtype, is characterized by exaggerated eosinophilic respiratory inflammation and reactions to aspirin, each involving the marked overproduction of cysLTs. Here we demonstrate that the type 2 cysLT receptor (CysLT2R), which is not targeted by available drugs, is required in two different models to amplify eosinophilic airway inflammation via induced expression of IL-33 by lung epithelial cells. Endogenously generated cysLTs induced eosinophilia and expanded group 2 innate lymphoid cells (ILC2s) in aspirin-exacerbated respiratory disease\u2013like Ptges\u2212\/\u2212 mice. These responses were mitigated by deletions of either Cysltr2 or leukotriene C4 synthase (Ltc4s). Administrations of either LTC4 (the parent cysLT) or the selective CysLT2R agonist N-methyl LTC4 to allergen sensitized wild-type mice markedly boosted ILC2 expansion and IL-5\/IL-13 generation in a CysLT2R-dependent manner. Expansion of ILC2s and IL-5\/IL-13 generation reflected CysLT2R-dependent production of IL-33 by alveolar type 2 cells, which engaged in a bilateral feed-forward loop with ILC2s. Deletion of Cysltr1 blunted LTC4-induced ILC2 expansion and eosinophilia but did not alter IL-33 induction. Pharmacological blockade of CysLT2R prior to inhalation challenge of Ptges\u2212\/\u2212 mice with aspirin blocked IL-33\u2013dependent mast cell activation, mediator release, and changes in lung function. Thus, CysLT2R signaling, IL-33\u2013dependent ILC2 expansion, and IL-33\u2013driven mast cell activation are necessary for induction of type 2 immunopathology and aspirin sensitivity. CysLT2R-targeted drugs may interrupt these processes.<\/jats:p>","DOI":"10.4049\/jimmunol.1700603","type":"journal-article","created":{"date-parts":[[2017,12,27]],"date-time":"2017-12-27T15:51:11Z","timestamp":1514389871000},"page":"915-927","source":"Crossref","is-referenced-by-count":69,"title":["Type 2 Cysteinyl Leukotriene Receptors Drive IL-33\u2013Dependent Type 2 Immunopathology and Aspirin Sensitivity"],"prefix":"10.1093","volume":"200","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1182-991X","authenticated-orcid":false,"given":"Tao","family":"Liu","sequence":"first","affiliation":[{"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 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nora A","family":"Barrett","sequence":"additional","affiliation":[{"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 02115"},{"name":"Department of Medicine, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshihide","family":"Kanaoka","sequence":"additional","affiliation":[{"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 02115"},{"name":"Department of Medicine, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0194-6845","authenticated-orcid":false,"given":"Eri","family":"Yoshimoto","sequence":"additional","affiliation":[{"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 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Denise","family":"Garofalo","sequence":"additional","affiliation":[{"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 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haley","family":"Cirka","sequence":"additional","affiliation":[{"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 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chunli","family":"Feng","sequence":"additional","affiliation":[{"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 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua A","family":"Boyce","sequence":"additional","affiliation":[{"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 02115"},{"name":"Department of Medicine, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2018,2,1]]},"reference":[{"key":"2025030610012497400_r1","doi-asserted-by":"crossref","first-page":"1105","DOI":"10.1084\/jem.20051615","article-title":"Identification of an interleukin (IL)-25-dependent cell population that provides IL-4, IL-5, and IL-13 at the onset of helminth expulsion","volume":"203","author":"Fallon","year":"2006","journal-title":"J. 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