| pubmed-article:16051830 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C0042776 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C0521026 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C0015980 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C1510506 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C1417530 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C0439677 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C1550548 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C1555714 | lld:lifeskim |
| pubmed-article:16051830 | lifeskim:mentions | umls-concept:C1705654 | lld:lifeskim |
| pubmed-article:16051830 | pubmed:issue | 16 | lld:pubmed |
| pubmed-article:16051830 | pubmed:dateCreated | 2005-7-29 | lld:pubmed |
| pubmed-article:16051830 | pubmed:abstractText | Alpha/beta interferons (IFN-alpha/beta) are key mediators of innate immunity and important modulators of adaptive immunity. The mechanisms by which IFN-alpha/beta are induced are becoming increasingly well understood. Recent studies showed that Toll-like receptors 7 and 8 expressed by plasmacytoid dendritic cells (pDCs) mediate the endosomal recognition of incoming viral RNA genomes, a process which requires myeloid differentiation factor 88 (MyD88). Here we investigate the requirements for virus-induced IFN-alpha/beta production in cultures of bone marrow-derived murine myeloid DCs (mDCs). Using recombinant Semliki Forest virus blocked at different steps in the viral life cycle, we show that replication-defective virus induced IFN-alpha/beta in mDCs while fusion-defective virus did not induce IFN-alpha/beta. The response to replication-defective virus was largely intact in MyD88-/- mDC cultures but was severely reduced in mDC cultures from mice lacking IFN regulatory factor 3. Our observations suggest that mDCs respond to incoming virus via a pathway that differs from the fusion-independent, MyD88-mediated endosomal pathway described for the induction of IFN-alpha/beta in pDCs. We propose that events during or downstream of viral fusion, but prior to replication, can activate IFN-alpha/beta in mDCs. Thus, mDCs may contribute to the antiviral response activated by the immune system at early time points after infection. | lld:pubmed |
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| pubmed-article:16051830 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16051830 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16051830 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16051830 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
