pubmed-article:18367527 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18367527 | lifeskim:mentions | umls-concept:C0682458 | lld:lifeskim |
pubmed-article:18367527 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:18367527 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
pubmed-article:18367527 | lifeskim:mentions | umls-concept:C0332466 | lld:lifeskim |
pubmed-article:18367527 | lifeskim:mentions | umls-concept:C1999216 | lld:lifeskim |
pubmed-article:18367527 | lifeskim:mentions | umls-concept:C0332261 | lld:lifeskim |
pubmed-article:18367527 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:18367527 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
pubmed-article:18367527 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:18367527 | pubmed:dateCreated | 2008-5-15 | lld:pubmed |
pubmed-article:18367527 | pubmed:abstractText | Dendritic cells (DCs) play a key role in innate immune responses, and their interactions with T cells are critical for the induction of adaptive immunity. However, immunodeficiency viruses are efficiently captured by DCs and can be transmitted to and amplified in CD4(+) T cells, with potentially deleterious effects on the induction of immune responses. In DC-T-cell cocultures, contact with CD4(+), not CD8(+), T cells preferentially facilitated virus movement to and release at immature and mature DC-T-cell contact sites. This occurred within 5 min of DC-T-cell contact. While the fusion inhibitor T-1249 did not prevent virus capture by DCs or the release of viruses at the DC-T-cell contact points, it readily blocked virus transfer to and amplification in CD4(+) T cells. Higher doses of T-1249 were needed to block the more robust replication driven by mature DCs. Virus accumulated in DCs within T-1249-treated cocultures but these DCs were actually less infectious than DCs isolated from untreated cocultures. Importantly, T-1249 did not interfere with the stimulation of virus-specific CD4(+) and CD8(+) T-cell responses when present during virus-loading of DCs or for the time of the DC-T-cell coculture. These results provide clues to identifying strategies to prevent DC-driven virus amplification in CD4(+) T cells while maintaining virus-specific immunity, an objective critical in the development of microbicides and therapeutic vaccines. | lld:pubmed |
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pubmed-article:18367527 | pubmed:language | eng | lld:pubmed |
pubmed-article:18367527 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18367527 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18367527 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:18367527 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18367527 | pubmed:month | Jun | lld:pubmed |
pubmed-article:18367527 | pubmed:issn | 1098-5514 | lld:pubmed |
pubmed-article:18367527 | pubmed:author | pubmed-author:RomanoPP | lld:pubmed |