{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T05:32:52Z","timestamp":1791091972043,"version":"4.1.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2011,10,1]],"date-time":"2011-10-01T00:00:00Z","timestamp":1317427200000},"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":[[2011,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Inhibiting allergic airway inflammation is the goal of therapy in persistent asthma. Administration of medication via the airways delivers drug directly to the site of inflammation and avoids systemic side effects but often fails to modulate systemic features of asthma. We have shown that Th1 cells, through production of IFN-\u03b3, inhibit many Th2-induced effector functions that promote disease. Using a newly generated mouse that expresses IFN-\u03b3R only on airway epithelial cells, we show that the airway epithelium controls a range of pathological responses in asthma. IFN-\u03b3 acting only through the airway epithelium inhibits mucus, chitinases, and eosinophilia, independent of Th2 cell activation. IFN-\u03b3 signaling through the airway epithelium inhibits eosinophil generation in the bone marrow, indicating that signals on the airway mucosal surface can regulate distant functions to inhibit disease. IFN-\u03b3 actions through the airway epithelium will limit airway obstruction and inflammation and may be therapeutic in refractory asthma.<\/jats:p>","DOI":"10.4049\/jimmunol.1100436","type":"journal-article","created":{"date-parts":[[2011,8,27]],"date-time":"2011-08-27T01:13:51Z","timestamp":1314407631000},"page":"3815-3820","source":"Crossref","is-referenced-by-count":87,"title":["IFN-\u03b3 Acts on the Airway Epithelium To Inhibit Local and Systemic Pathology in Allergic Airway Disease"],"prefix":"10.1093","volume":"187","author":[{"given":"Charlotte","family":"Mitchell","sequence":"first","affiliation":[{"name":"Section of Pulmonary and Critical Care, Yale University School of Medicine , New Haven, CT 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karin","family":"Provost","sequence":"additional","affiliation":[{"name":"Section of Pulmonary and Critical Care, Yale University School of Medicine , New Haven, CT 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naiqian","family":"Niu","sequence":"additional","affiliation":[{"name":"Section of Pulmonary and Critical Care, Yale University School of Medicine , New Haven, CT 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Homer","sequence":"additional","affiliation":[{"name":"Department of Pathology, Yale University School of Medicine , New Haven, CT 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren","family":"Cohn","sequence":"additional","affiliation":[{"name":"Section of Pulmonary and Critical Care, Yale University School of Medicine , New Haven, CT 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2011,10,1]]},"reference":[{"key":"2025032410384606100_r1","doi-asserted-by":"crossref","first-page":"298","DOI":"10.1056\/NEJM199201303260504","article-title":"Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma","volume":"326","author":"Robinson","year":"1992","journal-title":"N. 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