{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T11:50:59Z","timestamp":1790250659113,"version":"4.1.0"},"reference-count":30,"publisher":"Rockefeller University Press","issue":"1","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2002,1,7]]},"abstract":"<jats:p>Interleukin (IL)-9 is a pleiotropic cytokine secreted by T helper (Th)2 cells and has been proposed as a candidate gene for asthma and allergy. We have used mice genetically deficient in IL-9 to determine the role of this cytokine in the pathophysiologic features of the allergic pulmonary response\u2013airway hyperreactivity (AHR) and eosinophilia. We have demonstrated that IL-9 is not required for the development of a robust Th2 response to allergen in sensitized mice. IL-9 knockout mice developed a similar degree of eosinophilic inflammation and AHR to their wild-type littermates. Goblet cell hyperplasia and immunoglobulin (Ig) E production were also unaffected by the lack of IL-9. Moreover, levels of bronchoalveolar lavage (BAL) IL-4, IL-5, and IL-13 were comparable between wild-type and knockout mice. These findings indicate that IL-9 is not obligatory for the development of eosinophilia and AHR, and imply that other Th2 cytokines can act in a compensatory fashion.<\/jats:p>","DOI":"10.1084\/jem.20011732","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:48:33Z","timestamp":1027702113000},"page":"51-57","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":114,"title":["The Absence of Interleukin 9 Does Not Affect the Development of Allergen-induced Pulmonary Inflammation nor Airway Hyperreactivity"],"prefix":"10.1084","volume":"195","author":[{"given":"Sarah J.","family":"McMillan","sequence":"first","affiliation":[{"name":"1Leukocyte Biology Section, Division of Biomedical Sciences, Faculty of Medicine, Imperial College of Science, Technology, and Medicine, London SW7 2AZ, England"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin","family":"Bishop","sequence":"additional","affiliation":[{"name":"1Leukocyte Biology Section, Division of Biomedical Sciences, Faculty of Medicine, Imperial College of Science, Technology, and Medicine, London SW7 2AZ, England"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J.","family":"Townsend","sequence":"additional","affiliation":[{"name":"2Medical Research Council Laboratory for Molecular Biology, Cambridge CB2 2QH, England"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew N.","family":"McKenzie","sequence":"additional","affiliation":[{"name":"2Medical Research Council Laboratory for Molecular Biology, Cambridge CB2 2QH, England"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clare M.","family":"Lloyd","sequence":"additional","affiliation":[{"name":"1Leukocyte Biology Section, Division of Biomedical Sciences, Faculty of Medicine, Imperial College of Science, Technology, and Medicine, London SW7 2AZ, England"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2002,1,7]]},"reference":[{"key":"2023072511223061200_BIB1","doi-asserted-by":"crossref","first-page":"610","DOI":"10.1016\/S0952-7915(99)00025-4","volume":"11","year":"1999","journal-title":"Curr. 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