| pubmed-article:16641270 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16641270 | lifeskim:mentions | umls-concept:C0086427 | lld:lifeskim |
| pubmed-article:16641270 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:16641270 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:16641270 | lifeskim:mentions | umls-concept:C0913092 | lld:lifeskim |
| pubmed-article:16641270 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
| pubmed-article:16641270 | lifeskim:mentions | umls-concept:C0332466 | lld:lifeskim |
| pubmed-article:16641270 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:16641270 | pubmed:dateCreated | 2006-4-27 | lld:pubmed |
| pubmed-article:16641270 | pubmed:abstractText | Interactions between the oncogenic retrovirus human T-cell leukemia virus type 1 (HTLV-1) and dendritic cells (DCs) are poorly characterized. We show here that monocyte-derived DCs form syncytia and are infected upon coculture with HTLV-1-infected lymphocytes. We examined the role of DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN), a C-type lectin expressed in DCs, in HTLV-1-induced syncytium formation. DC-SIGN is known to bind with high affinity to various viral envelope glycoproteins, including human immunodeficiency virus (HIV) and hepatitis C virus, as well as to the cellular receptors ICAM-2 and ICAM-3. After cocultivating DCs and HTLV-1-infected cells, we found that anti-DC-SIGN monoclonal antibodies (MAbs) were able to decrease the number and size of HTLV-1-induced syncytia. Moreover, expression of the lectin in epithelial-cell lines dramatically enhanced the ability to fuse with HTLV-1-positive cells. Interestingly, in contrast to the envelope (Env) glycoproteins of HIV and other viruses, that of HTLV-1 does not bind directly to DC-SIGN. The facilitating role of the lectin in HTLV-1 syncytium formation is mediated by its interaction with ICAM-2 and ICAM-3, as demonstrated by use of MAbs directed against these adhesion molecules. Altogether, our results indicate that DC-SIGN facilitates HTLV-1 infection and fusion of DCs through an ICAM-dependent mechanism. | lld:pubmed |
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| pubmed-article:16641270 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16641270 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16641270 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16641270 | pubmed:month | May | lld:pubmed |
| pubmed-article:16641270 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:16641270 | pubmed:author | pubmed-author:AbastadoJean-... | lld:pubmed |
| pubmed-article:16641270 | pubmed:author | pubmed-author:GessainAntoin... | lld:pubmed |
| pubmed-article:16641270 | pubmed:author | pubmed-author:MorisArnaudA | lld:pubmed |
| pubmed-article:16641270 | pubmed:author | pubmed-author:SchwartzOlivi... | lld:pubmed |
| pubmed-article:16641270 | pubmed:author | pubmed-author:OzdenSimonaS | lld:pubmed |
| pubmed-article:16641270 | pubmed:author | pubmed-author:PrevostMarie-... | lld:pubmed |
| pubmed-article:16641270 | pubmed:author | pubmed-author:DelebecqueFré... | lld:pubmed |
| pubmed-article:16641270 | pubmed:author | pubmed-author:CeccaldiPierr... | lld:pubmed |
| pubmed-article:16641270 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16641270 | pubmed:volume | 80 | lld:pubmed |
| pubmed-article:16641270 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16641270 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16641270 | pubmed:pagination | 4771-80 | lld:pubmed |
| pubmed-article:16641270 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:16641270 | pubmed:meshHeading | pubmed-meshheading:16641270... | lld:pubmed |
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| pubmed-article:16641270 | pubmed:meshHeading | pubmed-meshheading:16641270... | lld:pubmed |
| pubmed-article:16641270 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16641270 | pubmed:articleTitle | DC-SIGN facilitates fusion of dendritic cells with human T-cell leukemia virus type 1-infected cells. | lld:pubmed |
| pubmed-article:16641270 | pubmed:affiliation | Unité Epidémiologie et Physiopathologie des Virus Oncogènes, Institut Pasteur, Paris Cedex 15, France. | lld:pubmed |
| pubmed-article:16641270 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16641270 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
