{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T23:04:15Z","timestamp":1776121455148,"version":"3.50.1"},"reference-count":40,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2007,8,28]],"date-time":"2007-08-28T00:00:00Z","timestamp":1188259200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2007,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Background\n\t\t\t\t\t<\/jats:bold> T\u2010helper type 2 (Th2)\u2010derived cytokines such as IL\u20104, IL\u20105, IL\u20109 and IL\u201013 play an important role in the synthesis of IgE and in the promotion of allergic eosinophilic inflammation and airway wall remodelling.<\/jats:p><jats:p><jats:bold>Objective\n\t\t\t\t\t<\/jats:bold> We determined the importance of IL\u201013 alone, and of the four Th2 cytokines together, by studying mice in which either IL\u201013 alone or the Th2 cytokine cluster was genetically disrupted.<\/jats:p><jats:p><jats:bold>Methods\n\t\t\t\t\t<\/jats:bold> The knock\u2010out mice and their BALB\/c wild\u2010type (wt) counterparts were sensitized and repeatedly exposed to ovalbumin (OVA) aerosol.<\/jats:p><jats:p><jats:bold>Results\n\t\t\t\t\t<\/jats:bold> Bronchial responsiveness measured as the concentration of acetylcholine aerosol needed to increase baseline lung resistance by 100% (PC<jats:sub>100<\/jats:sub>) was decreased in IL\u201013<jats:sup>\u2212\/\u2212<\/jats:sup>, but increased in IL\u20104\/5\/9\/13<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Chronic allergen exposure resulted in airway hyperresponsiveness (AHR) in wt mice but not in both genetically modified mice. After allergen exposure, eosinophil counts in bronchoalveolar lavage fluid and in airways mucosa, and goblet cell numbers were not increased in IL\u20104\/5\/9\/13<jats:sup>\u2212\/\u2212<\/jats:sup> mice, and were only attenuated in IL\u201013<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Airway smooth muscle (ASM) hyperplasia after allergen exposure was prevented in both IL\u201013<jats:sup>\u2212\/\u2212<\/jats:sup> and IL\u20104\/5\/9\/13<jats:sup>\u2212\/\u2212<\/jats:sup> mice to an equal extent. Similarly, the rise in total or OVA\u2010specific serum IgE levels was totally inhibited.<\/jats:p><jats:p><jats:bold>Conclusion\n\t\t\t\t\t<\/jats:bold> IL\u201013 is mainly responsible for AHR, ASM hyperplasia and increases in IgE, while IL\u20104, \u20105 and \u20109 may contribute to goblet cell hyperplasia and eosinophilic inflammation induced by chronic allergen exposure in a murine model. Both redundancy or complementariness of Th2 cytokines can occur <jats:italic>in vivo<\/jats:italic>, according to specific aspects of the allergic response.<\/jats:p>","DOI":"10.1111\/j.1365-2222.2007.02789.x","type":"journal-article","created":{"date-parts":[[2007,9,1]],"date-time":"2007-09-01T04:11:21Z","timestamp":1188619881000},"page":"1427-1435","source":"Crossref","is-referenced-by-count":36,"title":["Complete inhibition of allergic airway inflammation and remodelling in quadruple IL\u20104\/5\/9\/13<sup>\u2212\/\u2212<\/sup> mice"],"prefix":"10.1111","volume":"37","author":[{"given":"Puneeta","family":"Nath","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sum","family":"Yee Leung","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alison S.","family":"Williams","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alistair","family":"Noble","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shaoping","family":"Xie","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew N. 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