| pubmed-article:17506035 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17506035 | lifeskim:mentions | umls-concept:C0024109 | lld:lifeskim |
| pubmed-article:17506035 | lifeskim:mentions | umls-concept:C0004096 | lld:lifeskim |
| pubmed-article:17506035 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17506035 | lifeskim:mentions | umls-concept:C0458827 | lld:lifeskim |
| pubmed-article:17506035 | lifeskim:mentions | umls-concept:C0882784 | lld:lifeskim |
| pubmed-article:17506035 | lifeskim:mentions | umls-concept:C1414234 | lld:lifeskim |
| pubmed-article:17506035 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:17506035 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
| pubmed-article:17506035 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:17506035 | pubmed:dateCreated | 2007-5-29 | lld:pubmed |
| pubmed-article:17506035 | pubmed:abstractText | Epstein-Barr virus-induced gene (EBI)-3 codes for a soluble type 1 cytokine receptor homologous to the p40 subunit of IL-12 that is expressed by antigen-presenting cells following activation. Here, we analyzed the functional role of EBI-3 in a murine model of asthma associated with airway hyper-responsiveness (AHR) in ovalbumin-sensitized mice. Upon allergen challenge, EBI-3-/- mice showed less severe AHR, decreased numbers and degranulation of eosinophils and a significantly reduced number of VCAM-1+ cells in the lungs as compared to wild-type littermates. We thus analyzed lung CD11c+ cells before and after allergen challenge in these mice and found that before allergen challenge, lung CD11c+ cells isolated from EBI-3-/- mice express markers of a more plasmacytoid phenotype without releasing IFN-alpha as compared to those from wild-type littermates. Moreover, allergen challenge induced the development of myeloid CD11c+ cells in the lungs of EBI-3-/- mice, which released increased amounts of IL-10 and IL-12 while not expressing IFN-alpha. Finally, inhibition of EBI-3 expression in lung DC could prevent AHR in adoptive transfer studies by suppressing mediator release of effector cells into the airways. These results indicate a novel role for EBI-3 in controlling local immune responses in the lungs in experimental asthma. | lld:pubmed |
| pubmed-article:17506035 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17506035 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17506035 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17506035 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:17506035 | pubmed:issn | 0014-2980 | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:GallePeter... | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:NeurathMarkus... | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:FinottoSusett... | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:LehrHans AHA | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:BlumbergRicha... | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:RenzHaraldH | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:BirkenbachMar... | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:ScholtesPetra... | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:HausdingMicha... | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:WegmannMichae... | lld:pubmed |
| pubmed-article:17506035 | pubmed:author | pubmed-author:KarwotRomanR | lld:pubmed |
| pubmed-article:17506035 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17506035 | pubmed:volume | 37 | lld:pubmed |
| pubmed-article:17506035 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17506035 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17506035 | pubmed:pagination | 1663-77 | lld:pubmed |
| pubmed-article:17506035 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:17506035 | pubmed:meshHeading | pubmed-meshheading:17506035... | lld:pubmed |
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| pubmed-article:17506035 | pubmed:meshHeading | pubmed-meshheading:17506035... | lld:pubmed |
| pubmed-article:17506035 | pubmed:meshHeading | pubmed-meshheading:17506035... | lld:pubmed |
| pubmed-article:17506035 | pubmed:meshHeading | pubmed-meshheading:17506035... | lld:pubmed |
| pubmed-article:17506035 | pubmed:meshHeading | pubmed-meshheading:17506035... | lld:pubmed |
| pubmed-article:17506035 | pubmed:meshHeading | pubmed-meshheading:17506035... | lld:pubmed |
| pubmed-article:17506035 | pubmed:meshHeading | pubmed-meshheading:17506035... | lld:pubmed |
| pubmed-article:17506035 | pubmed:meshHeading | pubmed-meshheading:17506035... | lld:pubmed |
| pubmed-article:17506035 | pubmed:meshHeading | pubmed-meshheading:17506035... | lld:pubmed |
| pubmed-article:17506035 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17506035 | pubmed:articleTitle | Lung CD11c+ cells from mice deficient in Epstein-Barr virus-induced gene 3 (EBI-3) prevent airway hyper-responsiveness in experimental asthma. | lld:pubmed |
| pubmed-article:17506035 | pubmed:affiliation | Laboratory of Cellular and Molecular Lung Immunology, I Medical Clinic, University of Mainz, Mainz, Germany, and Institut Universitaire de Pathologie Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. | lld:pubmed |
| pubmed-article:17506035 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17506035 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:50498 | entrezgene:pubmed | pubmed-article:17506035 | lld:entrezgene |
