| pubmed-article:16327802 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16327802 | lifeskim:mentions | umls-concept:C0214743 | lld:lifeskim |
| pubmed-article:16327802 | lifeskim:mentions | umls-concept:C1704256 | lld:lifeskim |
| pubmed-article:16327802 | lifeskim:mentions | umls-concept:C0016059 | lld:lifeskim |
| pubmed-article:16327802 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:16327802 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:16327802 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:16327802 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:16327802 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:16327802 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:16327802 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:16327802 | pubmed:dateCreated | 2006-1-6 | lld:pubmed |
| pubmed-article:16327802 | pubmed:abstractText | Interleukin (IL)-13 is a major inducer of fibrosis in many chronic infectious and autoimmune diseases. In studies of the mechanisms underlying such induction, we found that IL-13 induces transforming growth factor (TGF)-beta(1) in macrophages through a two-stage process involving, first, the induction of a receptor formerly considered to function only as a decoy receptor, IL-13Ralpha(2). Such induction requires IL-13 (or IL-4) and tumor necrosis factor (TNF)-alpha. Second, it involves IL-13 signaling through IL-13Ralpha(2) to activate an AP-1 variant containing c-jun and Fra-2, which then activates the TGFB1 promoter. In vivo, we found that prevention of IL-13Ralpha(2) expression reduced production of TGF-beta(1) in oxazolone-induced colitis and that prevention of IL-13Ralpha(2) expression, Il13ra2 gene silencing or blockade of IL-13Ralpha(2) signaling led to marked downregulation of TGF-beta(1) production and collagen deposition in bleomycin-induced lung fibrosis. These data suggest that IL-13Ralpha(2) signaling during prolonged inflammation is an important therapeutic target for the prevention of TGF-beta(1)-mediated fibrosis. | lld:pubmed |
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| pubmed-article:16327802 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16327802 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16327802 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:16327802 | pubmed:issn | 1078-8956 | lld:pubmed |
| pubmed-article:16327802 | pubmed:author | pubmed-author:StroberWarren... | lld:pubmed |
| pubmed-article:16327802 | pubmed:author | pubmed-author:KawakamiKojiK | lld:pubmed |
| pubmed-article:16327802 | pubmed:author | pubmed-author:PuriRaj KRK | lld:pubmed |
| pubmed-article:16327802 | pubmed:author | pubmed-author:KitaniAtsushi... | lld:pubmed |
| pubmed-article:16327802 | pubmed:author | pubmed-author:Fichtner-Feig... | lld:pubmed |
| pubmed-article:16327802 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16327802 | pubmed:volume | 12 | lld:pubmed |
| pubmed-article:16327802 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16327802 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16327802 | pubmed:pagination | 99-106 | lld:pubmed |
| pubmed-article:16327802 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:16327802 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16327802 | pubmed:articleTitle | IL-13 signaling through the IL-13alpha2 receptor is involved in induction of TGF-beta1 production and fibrosis. | lld:pubmed |
| pubmed-article:16327802 | pubmed:affiliation | Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10-CRC 5W3864, 10 Center Drive, Bethesda, Maryland 20892, USA. | lld:pubmed |
| pubmed-article:16327802 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16327802 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
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