{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T12:46:01Z","timestamp":1787921161621,"version":"build-2784847793"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2001,2,1]],"date-time":"2001-02-01T00:00:00Z","timestamp":980985600000},"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":[[2001,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Airway eosinophilia in asthma is dependent on cytokines secreted by Th2 cells, including IL-5 and IL-4. In these studies we investigated why the absence of IL-4 led to a reduction in airway, but not lung tissue, eosinophils. Using adoptively transferred, in vitro-generated TCR-transgenic Th2 cells deficient in IL-4, we show that this effect is independent of IL-5 and Th2 cell generation. Airway eosinophilia was no longer inhibited when IL-4\u2212\/\u2212 Th2 cells were transferred into IFN-\u03b3R\u2212\/\u2212 mice, indicating that IFN-\u03b3 was responsible for reducing airway eosinophils in the absence of IL-4. Intranasal administration of IFN-\u03b3 to mice after IL-4+\/+ Th2 cell transfer also caused a reduction in airway, but not lung parenchymal, eosinophils. These studies show that IL-4 indirectly promotes airway eosinophilia by suppressing the production of IFN-\u03b3. IFN-\u03b3 reduces airway eosinophils by engaging its receptor on hemopoietic cells, possibly the eosinophil itself. These studies capitalize on the complex counterregulatory effects of Th1 and Th2 cytokines in vivo and clarify how IL-4 influences lung eosinophilia. We define a new regulatory role for IFN-\u03b3, demonstrating that eosinophilic inflammation is differentially regulated at distinct sites within the respiratory tract.<\/jats:p>","DOI":"10.4049\/jimmunol.166.4.2760","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T22:56:08Z","timestamp":1398034568000},"page":"2760-2767","source":"Crossref","is-referenced-by-count":70,"title":["IL-4 Promotes Airway Eosinophilia by Suppressing IFN-\u03b3 Production: Defining a Novel Role for IFN-\u03b3 in the Regulation of Allergic Airway Inflammation"],"prefix":"10.1093","volume":"166","author":[{"given":"Lauren","family":"Cohn","sequence":"first","affiliation":[{"name":"Sections of Pulmonary and Critical Care Medicine, Yale University School of Medicine , New Haven, CT 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina","family":"Herrick","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Yale University School of Medicine , New Haven, CT 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naiqian","family":"Niu","sequence":"additional","affiliation":[{"name":"Sections of Pulmonary and Critical Care Medicine, Yale University School of Medicine , New Haven, CT 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert J","family":"Homer","sequence":"additional","affiliation":[{"name":"Department of Pathology, Yale University School of Medicine , New Haven, CT 06520"},{"name":"Pathology and Laboratory Medicine Service, Veterans Affairs Connecticut Health Care System , West Haven, CT 06516"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kim","family":"Bottomly","sequence":"additional","affiliation":[{"name":"Immunobiology, Yale University School of Medicine , New Haven, CT 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2001,2,15]]},"reference":[{"key":"2026020209152370000_R1"},{"key":"2026020209152370000_R2","first-page":"1407","volume-title":"Am. 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