| pubmed-article:12515809 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12515809 | lifeskim:mentions | umls-concept:C0026912 | lld:lifeskim |
| pubmed-article:12515809 | lifeskim:mentions | umls-concept:C0913092 | lld:lifeskim |
| pubmed-article:12515809 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
| pubmed-article:12515809 | lifeskim:mentions | umls-concept:C0007613 | lld:lifeskim |
| pubmed-article:12515809 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
| pubmed-article:12515809 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:12515809 | pubmed:dateCreated | 2003-1-7 | lld:pubmed |
| pubmed-article:12515809 | pubmed:abstractText | Mycobacterium tuberculosis represents a world-wide health risk and immunosuppression is a particular problem in M. tuberculosis infections. Although macrophages are primarily infected, dendritic cells (DCs) are important in inducing cellular immune responses against M. tuberculosis. We hypothesized that DCs represent a target for M. tuberculosis and that the observed immuno-suppression results from modulation of DC functions. We demonstrate that the DC-specific C-type lectin DC-SIGN is an important receptor on DCs that captures and internalizes intact Mycobacterium bovis bacillus Calmette-Guérin (BCG) through the mycobacterial cell wall component ManLAM. Antibodies against DC-SIGN block M. bovis BCG infection of DCs. ManLAM is also secreted by M. tuberculosis-infected macrophages and has been implicated as a virulence factor. Strikingly, ManLAM binding to DC-SIGN prevents mycobacteria- or LPS-induced DC maturation. Both mycobacteria and LPS induce DC maturation through Toll-like receptor (TLR) signaling, suggesting that DC-SIGN, upon binding of ManLAM, interferes with TLR-mediated signals. Blocking antibodies against DC-SIGN reverse the ManLAM-mediated immunosuppressive effects. Our results suggest that M. tuberculosis targets DC-SIGN both to infect DCs and to down-regulate DC-mediated immune responses. Moreover, we demonstrate that DC-SIGN has a broader pathogen recognition profile than previously shown, suggesting that DC-SIGN may represent a molecular target for clinical intervention in infections other than HIV-1. | lld:pubmed |
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| pubmed-article:12515809 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12515809 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12515809 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12515809 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12515809 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:12515809 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:12515809 | pubmed:author | pubmed-author:GeijtenbeekTe... | lld:pubmed |
| pubmed-article:12515809 | pubmed:author | pubmed-author:Van... | lld:pubmed |
| pubmed-article:12515809 | pubmed:author | pubmed-author:Van... | lld:pubmed |
| pubmed-article:12515809 | pubmed:author | pubmed-author:KoppelEstella... | lld:pubmed |
| pubmed-article:12515809 | pubmed:author | pubmed-author:Sanchez-Herna... | lld:pubmed |
| pubmed-article:12515809 | pubmed:author | pubmed-author:Vandenbroucke... | lld:pubmed |
| pubmed-article:12515809 | pubmed:author | pubmed-author:AppelmelkBenB | lld:pubmed |
| pubmed-article:12515809 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12515809 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:12515809 | pubmed:volume | 197 | lld:pubmed |
| pubmed-article:12515809 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12515809 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12515809 | pubmed:pagination | 7-17 | lld:pubmed |
| pubmed-article:12515809 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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