{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T00:16:59Z","timestamp":1772929019608,"version":"3.50.1"},"reference-count":48,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2006,8,1]],"date-time":"2006-08-01T00:00:00Z","timestamp":1154390400000},"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":[[2006,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Generalized underrepresentation of IFN-\u03b3 has been implicated in the development of allergic asthma. However, the role of local IFN-\u03b3 in the lung during the development of this disease has not been completely elucidated. We studied the influence of local pulmonary IFN-\u03b3 expression on the development of allergen-induced lung inflammation. To restrict our analysis to IFN-\u03b3 expression in the lung and to exclude influences of systemic IFN-\u03b3 production, we generated a transgenic mouse line with a targeted deletion of the IFN-\u03b3 gene and constitutive, lung-specific IFN-\u03b3 expression (Clara cell 10 [CC10]\u2013IFN-\u03b3\u2013tg\u2013IFN-\u03b3\u2013KO mice), and compared allergen-induced airway inflammation in these mice with that of wild-type and IFN-\u03b3\u2013 KO mice on the C57BL\/6 background. Cytokine quantification in lungs of mice with allergic airway inflammation revealed that pulmonary IFN-\u03b3 expression increased expression of IL-5 and IL-13. Consistent with this observation, eosinophilia in bronchoalveolar lavage of CC10\u2013IFN-\u03b3\u2013tg\u2013IFN-\u03b3\u2013KO mice was profoundly increased, indicating that this critical component of asthma is enhanced by local IFN-\u03b3 expression. In contrast, airway hyperresponsiveness and anti-ovalbumin-IgE serum levels were reduced by local IFN-\u03b3 expression. Together, our results demonstrate pleiotropic action of constitutive IFN-\u03b3 expression in the lung, and question the therapeutic value of IFN-\u03b3 in allergic asthma. Local expression of IFN-\u03b3 in the lung increases markers of allergic airway inflammation, but decreases airway hyperresponsiveness in a murine model of allergic-asthma<\/jats:p>","DOI":"10.1165\/rcmb.2005-0293oc","type":"journal-article","created":{"date-parts":[[2006,3,16]],"date-time":"2006-03-16T20:45:19Z","timestamp":1142541919000},"page":"211-219","source":"Crossref","is-referenced-by-count":30,"title":["Role of Local Pulmonary IFN-\u03b3 Expression in Murine Allergic Airway Inflammation"],"prefix":"10.1093","volume":"35","author":[{"given":"Markus","family":"Koch","sequence":"first","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology, Berlin; Department of Internal Medicine, Charite, Humboldt-University, Berlin, Germany; and Division of Life Sciences, Kings College London, London, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin","family":"Witzenrath","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology, Berlin; Department of Internal Medicine, Charite, Humboldt-University, Berlin, Germany; and Division of Life Sciences, Kings College London, London, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christine","family":"Reuter","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology, Berlin; Department of Internal Medicine, Charite, Humboldt-University, Berlin, Germany; and Division of Life Sciences, Kings College London, London, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marion","family":"Herma","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology, Berlin; Department of Internal Medicine, Charite, Humboldt-University, Berlin, Germany; and Division of Life Sciences, Kings College London, London, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hartwig","family":"Sch\u00fctte","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology, Berlin; Department of Internal Medicine, Charite, Humboldt-University, Berlin, Germany; and Division of Life Sciences, Kings College London, London, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Norbert","family":"Suttorp","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology, Berlin; Department of Internal Medicine, Charite, Humboldt-University, Berlin, Germany; and Division of Life Sciences, Kings College London, London, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Helen","family":"Collins","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology, Berlin; Department of Internal Medicine, Charite, Humboldt-University, Berlin, Germany; and Division of Life Sciences, Kings College London, London, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefan H. 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