| pubmed-article:10727461 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10727461 | lifeskim:mentions | umls-concept:C0162351 | lld:lifeskim |
| pubmed-article:10727461 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:10727461 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:10727461 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:10727461 | lifeskim:mentions | umls-concept:C0040661 | lld:lifeskim |
| pubmed-article:10727461 | lifeskim:mentions | umls-concept:C1705162 | lld:lifeskim |
| pubmed-article:10727461 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:10727461 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:10727461 | pubmed:dateCreated | 2000-4-4 | lld:pubmed |
| pubmed-article:10727461 | pubmed:abstractText | Contact hypersensitivity (CHS) is thought to be mainly associated with the activation of T helper type 1 (Th1) cells. However, there is also evidence that Th2 cells or Th2 cytokines play a role in the development of CHS. To analyze the functional contribution of Th2 cytokines interleukin (IL)-4 and IL-13, signal transducer and activator of transcription 6 (STAT6)-deficient (STAT6(-/)-) and wild-type (wt) control C57BL/6 mice were contact sensitized with 5% 2,4,6-trinitrochlorobenzene (TNCB), 0.5% 2,4-dinitrofluorobenzene, or 5% 4-ethoxyl methylene-2-phenyl-2-oxazolin-5-one, and any skin reactions were examined. Ear swelling was significantly reduced with a delayed peak response in STAT6(-/)- mice compared with wt mice.A histological analysis revealed that the infiltration of both eosinophils and neutrophils in the skin challenged after 24 h in STAT6(-/)- mice decreased substantially compared with that in wt mice. The expression of Th2 cytokines (IL-4, IL-5) in TNCB-challenged skin tissues and the supernatants from T cells stimulated by 2,4,6-trinitrobenzene sulfonate-modified spleen cells, as well as the immunoglobulin (Ig)E and IgG1 response after challenge, were also profoundly reduced in STAT6(-/)- mice, whereas the expression of interferon gamma was the same in STAT6(-/)- and wt mice after challenge. Furthermore, adoptive transfer experiments revealed that STAT6(-/)- mice induced CHS after injection of lymph node cells obtained from sensitized wt mice. Our data suggest that the STAT6 signal plays a critical role in the induction phase of CHS. | lld:pubmed |
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| pubmed-article:10727461 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10727461 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10727461 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10727461 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10727461 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:10727461 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:10727461 | pubmed:author | pubmed-author:TakedaKK | lld:pubmed |
| pubmed-article:10727461 | pubmed:author | pubmed-author:TakayamaKK | lld:pubmed |
| pubmed-article:10727461 | pubmed:author | pubmed-author:KatayamaII | lld:pubmed |
| pubmed-article:10727461 | pubmed:author | pubmed-author:NishiokaKK | lld:pubmed |
| pubmed-article:10727461 | pubmed:author | pubmed-author:SatohTT | lld:pubmed |
| pubmed-article:10727461 | pubmed:author | pubmed-author:AkiraSS | lld:pubmed |
| pubmed-article:10727461 | pubmed:author | pubmed-author:YokozekiHH | lld:pubmed |
| pubmed-article:10727461 | pubmed:author | pubmed-author:TakagawaSS | lld:pubmed |
| pubmed-article:10727461 | pubmed:author | pubmed-author:GhoreishiMM | lld:pubmed |
| pubmed-article:10727461 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10727461 | pubmed:day | 20 | lld:pubmed |
| pubmed-article:10727461 | pubmed:volume | 191 | lld:pubmed |
| pubmed-article:10727461 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10727461 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10727461 | pubmed:pagination | 995-1004 | lld:pubmed |
| pubmed-article:10727461 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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