| pubmed-article:12517968 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12517968 | lifeskim:mentions | umls-concept:C0029347 | lld:lifeskim |
| pubmed-article:12517968 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:12517968 | lifeskim:mentions | umls-concept:C0014257 | lld:lifeskim |
| pubmed-article:12517968 | lifeskim:mentions | umls-concept:C0162832 | lld:lifeskim |
| pubmed-article:12517968 | lifeskim:mentions | umls-concept:C0021747 | lld:lifeskim |
| pubmed-article:12517968 | lifeskim:mentions | umls-concept:C0596138 | lld:lifeskim |
| pubmed-article:12517968 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:12517968 | lifeskim:mentions | umls-concept:C1415900 | lld:lifeskim |
| pubmed-article:12517968 | lifeskim:mentions | umls-concept:C0449450 | lld:lifeskim |
| pubmed-article:12517968 | lifeskim:mentions | umls-concept:C0332158 | lld:lifeskim |
| pubmed-article:12517968 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12517968 | pubmed:dateCreated | 2003-1-8 | lld:pubmed |
| pubmed-article:12517968 | pubmed:abstractText | Purified monocytes infected with influenza A virus do not become mature dendritic cells (DCs) and they present viral peptides poorly to autologous memory T cells. In this study, we investigated whether influenza A-infected monocytes matured to DCs with a high capacity to stimulate T cells when they were infected with influenza A virus in a model tissue setting wherein they were cocultured with endothelium grown on a type I collagen matrix. Intercellular interactions with endothelium strongly promoted the Ag-presenting capacity of monocyte-derived cells infected with influenza A virus, and the heterologous coculture system also enhanced production of IFN-alpha by monocytes in the absence of plasmacytoid cells. Production of IFN-alpha in the presence of endothelium correlated with monocyte differentiation to mature DCs and their ability to stimulate proliferation and IFN-gamma production by autologous T cells. Monocyte-derived cells that developed into migratory DCs promoted proliferation of influenza A virus-specific CD4(+) and CD8(+) cells, whereas those that developed into macrophages promoted proliferation of CD8(+) T cells only. This onset of APC activity could be partially blocked with Ab to the IFN-alphabeta receptor when monocytes were infected with UV-treated virus, but neutralizing this pathway was inconsequential when monocytes were infected with live virus. Thus, type I IFN and direct contact with endothelium promote development of influenza A virus-presenting activity in monocyte-derived cells in a setting in which this differentiation does not depend on plasmacytoid cells. However, when infected with live influenza virus, the role of type I IFN in mediating differentiation and Ag-presenting capacity is expendable, apparently due to other mechanisms of virus-mediated activation. | lld:pubmed |
| pubmed-article:12517968 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12517968 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12517968 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12517968 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:12517968 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12517968 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12517968 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12517968 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12517968 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:12517968 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:12517968 | pubmed:author | pubmed-author:MoranThomas... | lld:pubmed |
| pubmed-article:12517968 | pubmed:author | pubmed-author:RandolphGwend... | lld:pubmed |
| pubmed-article:12517968 | pubmed:author | pubmed-author:QuChunfengC | lld:pubmed |
| pubmed-article:12517968 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12517968 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:12517968 | pubmed:volume | 170 | lld:pubmed |
| pubmed-article:12517968 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12517968 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12517968 | pubmed:pagination | 1010-8 | lld:pubmed |
| pubmed-article:12517968 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:12517968 | pubmed:meshHeading | pubmed-meshheading:12517968... | lld:pubmed |
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| pubmed-article:12517968 | pubmed:meshHeading | pubmed-meshheading:12517968... | lld:pubmed |
| pubmed-article:12517968 | pubmed:meshHeading | pubmed-meshheading:12517968... | lld:pubmed |
| pubmed-article:12517968 | pubmed:meshHeading | pubmed-meshheading:12517968... | lld:pubmed |
| pubmed-article:12517968 | pubmed:meshHeading | pubmed-meshheading:12517968... | lld:pubmed |
| pubmed-article:12517968 | pubmed:meshHeading | pubmed-meshheading:12517968... | lld:pubmed |
| pubmed-article:12517968 | pubmed:meshHeading | pubmed-meshheading:12517968... | lld:pubmed |
| pubmed-article:12517968 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12517968 | pubmed:articleTitle | Autocrine type I IFN and contact with endothelium promote the presentation of influenza A virus by monocyte-derived APC. | lld:pubmed |
| pubmed-article:12517968 | pubmed:affiliation | Carl C. Icahn Institute for Gene Therapy and Molecular Medicine, Mt. Sinai School of Medicine, New York, NY 10029, USA. | lld:pubmed |
| pubmed-article:12517968 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12517968 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12517968 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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