{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,13]],"date-time":"2023-10-13T09:51:53Z","timestamp":1697190713726},"reference-count":38,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2001,9,1]]},"abstract":"<jats:p>Overexpression of interleukin (IL)-5 by the airway epithelium in mice using the rat CC10 promoter (NJ.1726 line) leads to several histopathologies characteristic of human asthma, including airway hyperreactivity (AHR). We investigated the contribution of B and T cells, as well as CD4 expression, to the development of AHR in IL-5 transgenic mice. NJ.1726 mice on a T cell or CD4 knockout background, but not on a B cell knockout background, lost intrinsic AHR. These effects occurred without decreases in IL-5 or eosinophils. We further investigated the contribution of \u03b1<jats:sub>4<\/jats:sub>-integrin signaling to the development of AHR in IL-5 transgenic mice through the administration of anti-CD49d (\u03b1<jats:sub>4<\/jats:sub>-integrin) antibody (PS\/2). Administration of PS\/2 resulted in immediate (16-h) inhibition of AHR. The inhibition of AHR was not associated with a decrease in airway eosinophils. These studies demonstrate that, despite the presence of increased levels of IL-5 and eosinophils in the lungs of NJ.1726 mice, CD4<jats:sup>+<\/jats:sup>cells and \u03b1<jats:sub>4<\/jats:sub>-integrin signaling are necessary for the intrinsic AHR that develops in IL-5 transgenic mice.<\/jats:p>","DOI":"10.1152\/ajplung.2001.281.3.l653","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T21:10:22Z","timestamp":1514063422000},"page":"L653-L659","source":"Crossref","is-referenced-by-count":10,"title":["Intrinsic AHR in IL-5 transgenic mice is dependent on CD4<sup>+<\/sup>cells and CD49d-mediated signaling"],"prefix":"10.1152","volume":"281","author":[{"given":"Michael T.","family":"Borchers","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Crosby","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Justice","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Farmer","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E.","family":"Hines","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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