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| pubmed-article:18250457 | lifeskim:mentions | umls-concept:C0003451 | lld:lifeskim |
| pubmed-article:18250457 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:18250457 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:18250457 | lifeskim:mentions | umls-concept:C0021747 | lld:lifeskim |
| pubmed-article:18250457 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:18250457 | lifeskim:mentions | umls-concept:C1622742 | lld:lifeskim |
| pubmed-article:18250457 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:18250457 | pubmed:dateCreated | 2008-2-5 | lld:pubmed |
| pubmed-article:18250457 | pubmed:abstractText | Type III IFNs (IFN-lambda/IL-28/29) are cytokines with type I IFN-like antiviral activities, which remain poorly characterized. We herein show that most cell types expressed both types I and III IFNs after TLR stimulation or virus infection, whereas the ability of cells to respond to IFN-lambda was restricted to a narrow subset of cells, including plasmacytoid dendritic cells and epithelial cells. To examine the role of type III IFN in antiviral defense, we generated IL-28Ralpha-deficient mice. These mice were indistinguishable from wild-type mice with respect to clearance of a panel of different viruses, whereas mice lacking the type I IFN receptor (IFNAR(-/-)) were significantly impaired. However, the strong antiviral activity evoked by treatment of mice with TLR3 or TLR9 agonists was significantly reduced in both IL-28RA(-/-) and IFNAR(-/-) mice. The type I IFN receptor system has been shown to mediate positive feedback on IFN-alphabeta expression, and we found that the type I IFN receptor system also mediates positive feedback on IFN-lambda expression, whereas IL-28Ralpha signaling does not provide feedback on either type I or type III IFN expression in vivo. Finally, using bone-marrow chimeric mice we showed that TLR-activated antiviral defense requires expression of IL-28Ralpha only on nonhemopoietic cells. In this compartment, epithelial cells responded to IFN-lambda and directly restricted virus replication. Our data suggest type III IFN to target a specific subset of cells and to contribute to the antiviral response evoked by TLRs. | lld:pubmed |
| pubmed-article:18250457 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18250457 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18250457 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:18250457 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18250457 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:18250457 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:18250457 | pubmed:author | pubmed-author:StaeheliPeter... | lld:pubmed |
| pubmed-article:18250457 | pubmed:author | pubmed-author:ChenZhiZ | lld:pubmed |
| pubmed-article:18250457 | pubmed:author | pubmed-author:JensenUffe... | lld:pubmed |
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| pubmed-article:18250457 | pubmed:author | pubmed-author:ThomsenAllan... | lld:pubmed |
| pubmed-article:18250457 | pubmed:author | pubmed-author:Dagnaes-Hanse... | lld:pubmed |
| pubmed-article:18250457 | pubmed:author | pubmed-author:HartmannRuneR | lld:pubmed |
| pubmed-article:18250457 | pubmed:author | pubmed-author:AnkNinaN | lld:pubmed |
| pubmed-article:18250457 | pubmed:author | pubmed-author:KlucherKevinK | lld:pubmed |
| pubmed-article:18250457 | pubmed:author | pubmed-author:IversenMarie... | lld:pubmed |
| pubmed-article:18250457 | pubmed:author | pubmed-author:HaugenHaraldH | lld:pubmed |
| pubmed-article:18250457 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18250457 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:18250457 | pubmed:volume | 180 | lld:pubmed |
| pubmed-article:18250457 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18250457 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18250457 | pubmed:pagination | 2474-85 | lld:pubmed |
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| pubmed-article:18250457 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18250457 | pubmed:articleTitle | An important role for type III interferon (IFN-lambda/IL-28) in TLR-induced antiviral activity. | lld:pubmed |
| pubmed-article:18250457 | pubmed:affiliation | Institute of Medical Microbiology and Immunology, University of Aarhus, Aarhus, Denmark. | lld:pubmed |
| pubmed-article:18250457 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18250457 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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