{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T21:21:29Z","timestamp":1790889689466,"version":"4.1.0"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T00:00:00Z","timestamp":1172707200000},"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":[[2007,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Increased IL-9 expression, either systemically or under the control of lung-specific promoter, induces an asthma-like phenotype, including mucus overproduction, mastocytosis, lung eosinophilia, and airway hyperresponsiveness. These activities correlate with increased production of other Th2 cytokines such as IL-4, IL-5, and IL-13 in IL-9 Tg mice. To determine the exact role of IL-13 in this phenotype, mice overexpressing IL-9 were crossed with IL-13-deficient mice. In these animals, IL-9 could still induce mastocytosis and B lymphocyte infiltration of the lungs. Although IL-9-induced eosinophilia in the peritoneal cavity was not diminished in the absence of IL-13, IL-13 was required for IL-9 to increase eotaxin expression and lung eosinophilia. Mucus production and up-regulation of lung epithelial genes upon IL-9 overexpression were completely abolished in the absence of IL-13. Using hemopoietic cell transfer experiments with recipients that overexpressed IL-9 but were deficient in the IL-9 receptor (IL-9R), we could demonstrate that the effect of IL-9 on lung epithelial cells is indirect and could be fully restored by transfer of hemopoietic cells expressing IL-9R. Mucus production by lung epithelial cells was only up-regulated when hemopoietic cells simultaneously expressed functional IL-9R and IL-13 genes, indicating that IL-13 is not a cofactor but a direct mediator of the effect of IL-9 on lung epithelial cells. Taken together, these data indicate that IL-9 can promote asthma through IL-13-independent pathways via expansion of mast cells, eosinophils, and B cells, and through induction of IL-13 production by hemopoietic cells for mucus production and recruitment of eosinophils by lung epithelial cells.<\/jats:p>","DOI":"10.4049\/jimmunol.178.5.3244","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T13:14:39Z","timestamp":1397826879000},"page":"3244-3251","source":"Crossref","is-referenced-by-count":89,"title":["IL-13 Mediates In Vivo IL-9 Activities on Lung Epithelial Cells but Not on Hematopoietic Cells"],"prefix":"10.1093","volume":"178","author":[{"given":"Vale\u0301rie","family":"Steenwinckel","sequence":"first","affiliation":[{"name":"Ludwig Institute for Cancer Research and Experimental Medicine Unit, Universite\u0301 Catholique de Louvain , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jamila","family":"Louahed","sequence":"additional","affiliation":[{"name":"Ludwig Institute for Cancer Research and Experimental Medicine Unit, Universite\u0301 Catholique de Louvain , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ciriana","family":"Orabona","sequence":"additional","affiliation":[{"name":"Ludwig Institute for Cancer Research and Experimental Medicine Unit, Universite\u0301 Catholique de Louvain , Brussels ,","place":["Belgium"]},{"name":"Department of Experimental Medicine, University of Perugia , Perugia ,","place":["Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Franc\u0327ois","family":"Huaux","sequence":"additional","affiliation":[{"name":"Industrial Toxicology and Occupational Medicine Unit, Universite\u0301 Catholique de Louvain , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guy","family":"Warnier","sequence":"additional","affiliation":[{"name":"Ludwig Institute for Cancer Research and Experimental Medicine Unit, Universite\u0301 Catholique de Louvain , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"McKenzie","sequence":"additional","affiliation":[{"name":"Medical Research Council Laboratory of Molecular Biology , Hills Road, Cambridge ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dominique","family":"Lison","sequence":"additional","affiliation":[{"name":"Industrial Toxicology and Occupational Medicine Unit, Universite\u0301 Catholique de Louvain , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roy","family":"Levitt","sequence":"additional","affiliation":[{"name":"Genaera Corporation , Plymouth Meeting, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Christophe","family":"Renauld","sequence":"additional","affiliation":[{"name":"Ludwig Institute for Cancer Research and Experimental Medicine Unit, Universite\u0301 Catholique de Louvain , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2007,3,1]]},"reference":[{"key":"2026012810520227600_R1","first-page":"6934","volume-title":"Proc. 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