pubmed-article:14609571 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:14609571 | lifeskim:mentions | umls-concept:C0214743 | lld:lifeskim |
pubmed-article:14609571 | lifeskim:mentions | umls-concept:C1711178 | lld:lifeskim |
pubmed-article:14609571 | lifeskim:mentions | umls-concept:C0968296 | lld:lifeskim |
pubmed-article:14609571 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:14609571 | lifeskim:mentions | umls-concept:C1524075 | lld:lifeskim |
pubmed-article:14609571 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:14609571 | lifeskim:mentions | umls-concept:C0337112 | lld:lifeskim |
pubmed-article:14609571 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:14609571 | pubmed:dateCreated | 2003-11-11 | lld:pubmed |
pubmed-article:14609571 | pubmed:abstractText | Bronchial asthma is a complex disease characterized by airway inflammation involving Th2 cytokines. Among Th2 cytokines, the significance of IL-13 in the pathogenesis of bronchial asthma has recently emerged. Particularly, the direct action of IL-13 on bronchial epithelial cells (BECs) is critical for generation of airway hyperresponsiveness. IL-13 has two binding units; the IL-13 receptor alpha1 chain transduces the IL-13 signal comprising a heterodimer with the IL-4R alpha chain, whereas the IL-13 receptor alpha2 chain (IL-13Ralpha2) is thought to act as a decoy receptor. However, it remains obscure how expression of these molecules is regulated in each cell. In this article, we analyzed the expression of these components in BECs. Either IL-4 or IL-13 induced intracellular expression of IL-13Ralpha2 in BECs, which was STAT6-dependent and required de novo protein synthesis. IL-13Ralpha2 expressed on the cell surface as a monomer inhibited the STAT6-dependent IL-13 signal. Furthermore, expression of IL-13Ralpha2 was induced in lung tissues of ovalbumin-induced asthma model mice. Taken together, our results suggested the possibility that IL-13Ralpha2 induced by its ligand is transferred to the cell surface by an unknown mechanism, and it down-regulates the IL-13 signal in BECs, which functions as a unique negative-feedback system for the cytokine signal. | lld:pubmed |
pubmed-article:14609571 | pubmed:language | eng | lld:pubmed |
pubmed-article:14609571 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14609571 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:14609571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14609571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14609571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14609571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14609571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14609571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14609571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14609571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14609571 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:14609571 | pubmed:month | Dec | lld:pubmed |
pubmed-article:14609571 | pubmed:issn | 1043-4666 | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:TanakaHiroyuk... | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:YangQingQ | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:TodaShujiS | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:NagaiHiroichi... | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:SugitaYujiY | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:ArimaKazuhiko... | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:IzuharaKenjiK | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:MatsuiKeikoK | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:YuyamaNorikoN | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:MaedaMiyakoM | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:GodaChihoC | lld:pubmed |
pubmed-article:14609571 | pubmed:author | pubmed-author:YasunagaShin'... | lld:pubmed |
pubmed-article:14609571 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:14609571 | pubmed:day | 21 | lld:pubmed |
pubmed-article:14609571 | pubmed:volume | 24 | lld:pubmed |
pubmed-article:14609571 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:14609571 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:14609571 | pubmed:pagination | 293-303 | lld:pubmed |
pubmed-article:14609571 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:14609571 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:14609571 | pubmed:articleTitle | The negative-feedback regulation of the IL-13 signal by the IL-13 receptor alpha2 chain in bronchial epithelial cells. | lld:pubmed |
pubmed-article:14609571 | pubmed:affiliation | Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan. | lld:pubmed |
pubmed-article:14609571 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:14609571 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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