| pubmed-article:7479915 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7479915 | lifeskim:mentions | umls-concept:C0019682 | lld:lifeskim |
| pubmed-article:7479915 | lifeskim:mentions | umls-concept:C0017526 | lld:lifeskim |
| pubmed-article:7479915 | lifeskim:mentions | umls-concept:C0439640 | lld:lifeskim |
| pubmed-article:7479915 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:7479915 | lifeskim:mentions | umls-concept:C0080245 | lld:lifeskim |
| pubmed-article:7479915 | lifeskim:mentions | umls-concept:C1705630 | lld:lifeskim |
| pubmed-article:7479915 | pubmed:issue | 24 | lld:pubmed |
| pubmed-article:7479915 | pubmed:dateCreated | 1995-12-28 | lld:pubmed |
| pubmed-article:7479915 | pubmed:abstractText | Productive infection of T cells with human immunodeficiency virus 1 (HIV-1) typically requires that the T cells be stimulated with antigens or mitogens. This requirement has been attributed to the activation of the transcription factor NF-kappa B, which synergizes with the constitutive transcription factor Sp1 to drive the HIV-1 promoter. Recently, we have found that vigorous replication of HIV-1 takes place in nonactivated memory T cells after syncytium formation with dendritic cells (DCs). These syncytia lack activated cells as determined by an absence of staining for Ki-67 cell cycle antigen. The expression and activity of NF-kappa B and Sp1 were, therefore, analyzed in isolated T cells and DCs from humans and mice. We have used immunolabeling, Western blot analysis, and electrophoretic mobility shift and supershift assays. T cells lack active NF-kappa B but express Sp1 as expected. DCs express high levels of all known NF-kappa B and Rel proteins, with activity residing primarily within RelB, p50, and p65. However, DCs lack Sp1, which may explain the failure of HIV-1 to replicate in purified DCs. Coexpression of NF-kappa B and Sp1 occurs in the heterologous DC-T-cell syncytia that are induced by HIV-1. Therefore, HIV-1-induced cell fusion brings together factors that upregulate virus transcription. Since DCs and memory T cells frequently traffic together in situ, these unusual heterologous syncytia could develop in infected individuals and lead to chronic HIV-1 replication without ostensible immune stimulation. | lld:pubmed |
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| pubmed-article:7479915 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7479915 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7479915 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7479915 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:7479915 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:7479915 | pubmed:author | pubmed-author:Granelli-Pipe... | lld:pubmed |
| pubmed-article:7479915 | pubmed:author | pubmed-author:PopeMM | lld:pubmed |
| pubmed-article:7479915 | pubmed:author | pubmed-author:InabaKK | lld:pubmed |
| pubmed-article:7479915 | pubmed:author | pubmed-author:SteinmanR MRM | lld:pubmed |
| pubmed-article:7479915 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7479915 | pubmed:day | 21 | lld:pubmed |
| pubmed-article:7479915 | pubmed:volume | 92 | lld:pubmed |
| pubmed-article:7479915 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7479915 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7479915 | pubmed:pagination | 10944-8 | lld:pubmed |
| pubmed-article:7479915 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:7479915 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7479915 | pubmed:articleTitle | Coexpression of NF-kappa B/Rel and Sp1 transcription factors in human immunodeficiency virus 1-induced, dendritic cell-T-cell syncytia. | lld:pubmed |
| pubmed-article:7479915 | pubmed:affiliation | Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, NY 10021, USA. | lld:pubmed |
| pubmed-article:7479915 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7479915 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7479915 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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