{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T07:56:00Z","timestamp":1791014160279,"version":"4.1.0"},"reference-count":25,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2001,9,1]],"date-time":"2001-09-01T00:00:00Z","timestamp":999302400000},"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":[[2001,9,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Clara cell secretory protein (CC10) is a steroid-inducible protein, and its in vivo function is currently unclear. The role of CC10 in modulation of pulmonary allergic inflammation was examined in mice deficient for the CC10 gene. Wild-type and homozygous CC10-deficient mice were sensitized with an Ag, OVA, and challenged with either OVA or saline. When compared with that seen in wild-type mice, a significantly higher level of pulmonary eosinophilia was found in Ag-sensitized and challenged CC10-deficient mice. Significantly increased levels of Th2 cytokines IL-4, IL-5, IL-9, and IL-13 were also found in CC10-deficient mice. In addition, an increased level of eotaxin, but not RANTES, was also seen in CC10-deficient mice. No significant difference was observed in the level of a Th1 cytokine, IFN-\u03b3, between different groups of mice. These results provided the first in vivo evidence that CC10 plays a role in the modulation of pulmonary allergic inflammation.<\/jats:p>","DOI":"10.4049\/jimmunol.167.6.3025","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:30:26Z","timestamp":1398022226000},"page":"3025-3028","source":"Crossref","is-referenced-by-count":76,"title":["Cutting Edge: Altered Pulmonary Eosinophilic Inflammation in Mice Deficient for Clara Cell Secretory 10-kDa Protein"],"prefix":"10.1093","volume":"167","author":[{"given":"Li-Chen","family":"Chen","sequence":"first","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine , Baltimore, MD 21224"},{"name":"Division of Allergy, Asthma, and Rheumatology, Department of Pediatrics, Chang Gung Children\u2019s Hospital , Taoyuan, Taiwan ,","place":["Republic of China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongjian","family":"Zhang","sequence":"additional","affiliation":[{"name":"National Institute of Child Health and Development, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allen C","family":"Myers","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine , Baltimore, MD 21224"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shau-Ku","family":"Huang","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine , Baltimore, MD 21224"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2001,9,15]]},"reference":[{"key":"2026020208124782300_R1"},{"key":"2026020208124782300_R2","first-page":"S132","volume-title":"J. 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