{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T18:32:40Z","timestamp":1790015560068,"version":"4.0.1"},"reference-count":0,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2001,12,24]],"date-time":"2001-12-24T00:00:00Z","timestamp":1009152000000},"content-version":"vor","delay-in-days":602,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2000,5]]},"abstract":"Background<\/jats:title>The role of Immunoglobulin (Ig)E in inflammation is the subject of considerable study and a number of studies have shown conflicting evidence for its role in eosinophil recruitment and bronchial hyperresponsiveness in a number of murine models. The low affinity IgE receptor, CD23, is known to act as a negative regulator of IgE production and we have used knockout mice deficient in CD23 to investigate the role of IgE in eosinophil recruitment and bronchial hyperresponsiveness in a murine model of airway inflammation.<\/jats:p><\/jats:sec>Objective<\/jats:title>To study the role of the low affinity Fc\u03b5II receptor, CD23 in IgE production, lung inflammation and bronchial hyperresponsiveness.<\/jats:p><\/jats:sec>Methods<\/jats:title>Wild\u2010type and CD23 knockout C57Bl\/6 mice (CD23\u2212\/\u2212<\/jats:sup>) were immunized by intraperitoneal injection with ovalbumin on days 0 and 14 and challenged with aerosolized antigen on day 21 for a period of up to 1 week. Blood samples, bronchoalveolar lavage and lung tissue samples were obtained to determine serum IgE levels and inflammatory cell numbers, respectively. Furthermore, airway resistance was measured to increasing concentrations of aerosolized 5\u2010hydroxytryptamine in order to evaluate the effect of CD23 deficiency on bronchial hyperresponsiveness to antigen challenge.<\/jats:p><\/jats:sec>Results<\/jats:title>Sensitization of wild\u2010type C57Bl\/6 mice to ovalbumin resulted in elevated levels of total serum IgE and ovalbumin\u2010specific IgE, which was significantly augmented in CD23 knockout C57Bl\/6 mice (CD23\u2212\/\u2212<\/jats:sup>). A significant increase in the percentage of eosinophils recovered in bronchoalveolar lavage fluid from wild\u2010type and CD23\u2212\/\u2212<\/jats:sup> mice was observed 24\u2003h following 3 or 7 days aerosol exposure with ovalbumin (10\u2003mg\/mL). At 3 days, the increase in the percentage of eosinophils was significantly greater in CD23\u2212\/\u2212<\/jats:sup> groups. Immunohistochemical analysis of lungs sections revealed the presence of CD3+, CD4+ and CD23+ cells in wild\u2010type mice but a lack of immunofluorescence of CD23+ cells in CD23\u2212\/\u2212<\/jats:sup> mice. In wild\u2010type ovalbumin\u2010immunized mice, bronchial hyperresponsiveness to aerosolized 5\u2010hydroxytryptamine was observed following a 3\u2010day antigen challenge, which was significantly greater in CD23\u2212\/\u2212<\/jats:sup> ovalbumin\u2010immunized mice.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>These studies demonstrate that CD23\u2212\/\u2212<\/jats:sup> mice have increased capacity to produce IgE consistent with the view of a negative feedback role for membrane\u2010bound CD23 and under such conditions, may account for the greater numbers of eosinophils recruited to the airways and bronchial hyperresponsiveness observed following acute but not chronic antigen challenge.<\/jats:p><\/jats:sec>","DOI":"10.1046\/j.1365-2222.2000.00806.x","type":"journal-article","created":{"date-parts":[[2003,3,11]],"date-time":"2003-03-11T09:43:28Z","timestamp":1047375808000},"page":"728-738","source":"Crossref","is-referenced-by-count":29,"title":["The role of CD23 on allergen\u2010induced IgE levels, pulmonary eosinophilia and bronchial hyperresponsiveness in mice"],"prefix":"10.1111","volume":"30","author":[{"family":"Riffo\u2010Vasquez","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"family":"Spina","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"family":"Thomas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"family":"Gilbey","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"family":"Kemeny","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"family":"Page","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2001,12,24]]},"container-title":["Clinical & Experimental Allergy"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1046%2Fj.1365-2222.2000.00806.x","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1046%2Fj.1365-2222.2000.00806.x","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1046\/j.1365-2222.2000.00806.x","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,29]],"date-time":"2023-10-29T11:29:18Z","timestamp":1698578958000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1046\/j.1365-2222.2000.00806.x"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2000,5]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2000,5]]}},"alternative-id":["10.1046\/j.1365-2222.2000.00806.x"],"URL":"https:\/\/doi.org\/10.1046\/j.1365-2222.2000.00806.x","archive":["Portico"],"relation":{},"ISSN":["0954-7894","1365-2222"],"issn-type":[{"value":"0954-7894","type":"print"},{"value":"1365-2222","type":"electronic"}],"subject":[],"published":{"date-parts":[[2000,5]]}}}