| pubmed-article:15998792 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15998792 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:15998792 | lifeskim:mentions | umls-concept:C0033860 | lld:lifeskim |
| pubmed-article:15998792 | lifeskim:mentions | umls-concept:C1819431 | lld:lifeskim |
| pubmed-article:15998792 | lifeskim:mentions | umls-concept:C1548602 | lld:lifeskim |
| pubmed-article:15998792 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:15998792 | pubmed:dateCreated | 2005-7-6 | lld:pubmed |
| pubmed-article:15998792 | pubmed:abstractText | Psoriasis is one of the most common T cell-mediated autoimmune diseases in humans. Although a role for the innate immune system in driving the autoimmune T cell cascade has been proposed, its nature remains elusive. We show that plasmacytoid predendritic cells (PDCs), the natural interferon (IFN)-alpha-producing cells, infiltrate the skin of psoriatic patients and become activated to produce IFN-alpha early during disease formation. In a xenograft model of human psoriasis, we demonstrate that blocking IFN-alpha signaling or inhibiting the ability of PDCs to produce IFN-alpha prevented the T cell-dependent development of psoriasis. Furthermore, IFN-alpha reconstitution experiments demonstrated that PDC-derived IFN-alpha is essential to drive the development of psoriasis in vivo. These findings uncover a novel innate immune pathway for triggering a common human autoimmune disease and suggest that PDCs and PDC-derived IFN-alpha represent potential early targets for the treatment of psoriasis. | lld:pubmed |
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| pubmed-article:15998792 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15998792 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15998792 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15998792 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15998792 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:15998792 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:15998792 | pubmed:author | pubmed-author:BurgGünterG | lld:pubmed |
| pubmed-article:15998792 | pubmed:author | pubmed-author:HomeyBernhard... | lld:pubmed |
| pubmed-article:15998792 | pubmed:author | pubmed-author:LiuYong-JunYJ | lld:pubmed |
| pubmed-article:15998792 | pubmed:author | pubmed-author:GillietMichel... | lld:pubmed |
| pubmed-article:15998792 | pubmed:author | pubmed-author:Tun-KyiAdrian... | lld:pubmed |
| pubmed-article:15998792 | pubmed:author | pubmed-author:NestleFrank... | lld:pubmed |
| pubmed-article:15998792 | pubmed:author | pubmed-author:ConradCurdinC | lld:pubmed |
| pubmed-article:15998792 | pubmed:author | pubmed-author:BoymanOnurO | lld:pubmed |
| pubmed-article:15998792 | pubmed:author | pubmed-author:GombertMichae... | lld:pubmed |
| pubmed-article:15998792 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15998792 | pubmed:day | 4 | lld:pubmed |
| pubmed-article:15998792 | pubmed:volume | 202 | lld:pubmed |
| pubmed-article:15998792 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15998792 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15998792 | pubmed:pagination | 135-43 | lld:pubmed |
| pubmed-article:15998792 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:15998792 | pubmed:meshHeading | pubmed-meshheading:15998792... | lld:pubmed |
