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- Michael G. Brown
- Departments of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada
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- Laura L. Hermann
- Departments of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada
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- Andrew C. Issekutz
- Departments of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada
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- Jean S. Marshall
- Departments of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada
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- Derek Rowter
- Pediatrics, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada
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- Ayham Al-Afif
- Departments of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada
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- Robert Anderson
- Departments of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada
書誌事項
- 公開日
- 2011-01-15
- 権利情報
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- https://journals.asm.org/non-commercial-tdm-license
- DOI
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- 10.1128/jvi.01630-10
- 公開者
- American Society for Microbiology
この論文をさがす
説明
<jats:title>ABSTRACT</jats:title><jats:p>Vascular perturbation is a hallmark of severe forms of dengue disease. We show here that antibody-enhanced dengue virus infection of primary human cord blood-derived mast cells (CBMCs) and the human mast cell-like line HMC-1 results in the release of factor(s) which activate human endothelial cells, as evidenced by increased expression of the adhesion molecules ICAM-1 and VCAM-1. Endothelial cell activation was prevented by pretreatment of mast cell-derived supernatants with a tumor necrosis factor (TNF)-specific blocking antibody, thus identifying TNF as the endothelial cell-activating factor. Our findings suggest that mast cells may represent an important source of TNF, promoting vascular endothelial perturbation following antibody-enhanced dengue virus infection.</jats:p>
収録刊行物
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- Journal of Virology
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Journal of Virology 85 (2), 1145-1150, 2011-01-15
American Society for Microbiology