{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T11:42:57Z","timestamp":1790422977358,"version":"4.1.0"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"3","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":[[2001,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>In the mucosal immune system, resident dendritic cells are specialized for priming Th2-polarized immunity, whereas the Ag-presenting activity of macrophages has been linked with the development of Th1 phenotype. As an immune switch toward Th1 can protect against Th2-mediated allergic response, this study investigated the capacity of lung macrophages to stimulate Th1 responses during the secondary exposure to inhaled allergen, thereby suppressing Th2-mediated allergic airway inflammation in a murine model of allergic asthma. Following airway macrophage depletion in OVA-sensitized mice, lung T cells defaulted to a phenotype that produced less Th1 (IFN-\u03b3) and more Th2 (IL-4 and IL-5) cytokines, leading to more severe airway hyperreactivity and inflammation after intranasal Ag challenge. After OVA pulsing and adoptive transfer, lung macrophages selectively promoted a Th1 response in Ag-sensitized recipients and did not induce pulmonary eosinophilia. By contrast, OVA pulsing and adoptive transfer of a lung cell preparation, consisting of dendritic cells, B cells, and macrophages, promoted a Th2 response with an associated inflammatory response that was suppressed when macrophages were present and pretreated with IFN-\u03b3, but exacerbated when macrophages were depleted before IFN-\u03b3 treatment. In addition, Th1-promoting activity of lung macrophages was not related to the autocrine production of IL-12p40. These results suggest that the Th1-promoting APC activity may be an inherent property of the lung macrophage population, and may play an important role, upon stimulation by IFN-\u03b3, in antagonizing an ongoing Th2 immunity and Th2-dependent allergic responses.<\/jats:p>","DOI":"10.4049\/jimmunol.166.3.1471","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T21:55:06Z","timestamp":1398030906000},"page":"1471-1481","source":"Crossref","is-referenced-by-count":134,"title":["Th Type 1-Stimulating Activity of Lung Macrophages Inhibits Th2-Mediated Allergic Airway Inflammation by an IFN-\u03b3-Dependent Mechanism"],"prefix":"10.1093","volume":"166","author":[{"given":"Chibing","family":"Tang","sequence":"first","affiliation":[{"name":"Asthma Research Group, Department of Medicine, McMaster University , Hamilton, Ontario ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark D","family":"Inman","sequence":"additional","affiliation":[{"name":"Asthma Research Group, Department of Medicine, McMaster University , Hamilton, Ontario ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nico","family":"van Rooijen","sequence":"additional","affiliation":[{"name":"Department of Cell Biology and Immunology Faculty of Medicine, Vrije University , Amsterdam ,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pingchang","family":"Yang","sequence":"additional","affiliation":[{"name":"Asthma Research Group, Department of Medicine, McMaster University , Hamilton, Ontario ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huahao","family":"Shen","sequence":"additional","affiliation":[{"name":"Asthma Research Group, Department of Medicine, McMaster University , Hamilton, Ontario ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koichiro","family":"Matsumoto","sequence":"additional","affiliation":[{"name":"Asthma Research Group, Department of Medicine, McMaster University , Hamilton, Ontario ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul M","family":"O\u2019Byrne","sequence":"additional","affiliation":[{"name":"Asthma Research Group, Department of Medicine, McMaster University , Hamilton, Ontario ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2001,2,1]]},"reference":[{"key":"2026020209121289700_R1","first-page":"4090","volume-title":"J. 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