Cutting edge: paradoxical roles of BST2/tetherin in promoting type I IFN response and viral infection

Bone marrow stromal Ag 2 (BST2) is a transmembrane protein that prevents virus release from infected cells. It was also reported that BST2 inhibits type I IFN production by plasmacytoid dendritic cells. To determine BST2 impact on antiviral responses in vivo, we generated BST2(-/-) mice. Following i...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2012-03, Vol.188 (6), p.2488-2492
Main Authors: Swiecki, Melissa, Wang, Yaming, Gilfillan, Susan, Lenschow, Deborah J, Colonna, Marco
Format: Article
Language:English
Subjects:
Animals
Antigens, CD - immunology
Antigens, CD - metabolism
Cell Separation
Flow Cytometry
Interferon Type I - immunology
Interferon Type I - metabolism
Membrane Glycoproteins - immunology
Membrane Glycoproteins - metabolism
Mice
Mice, Knockout
Vesicular stomatitis virus
Virus Diseases - immunology
Virus Diseases - metabolism
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Summary:Bone marrow stromal Ag 2 (BST2) is a transmembrane protein that prevents virus release from infected cells. It was also reported that BST2 inhibits type I IFN production by plasmacytoid dendritic cells. To determine BST2 impact on antiviral responses in vivo, we generated BST2(-/-) mice. Following infection with a murine retrovirus, BST2(-/-) mice had slightly elevated viral loads; however, infection with other enveloped viruses revealed unexpected roles of BST2. BST2(-/-) mice showed reduced type I IFN production by plasmacytoid dendritic cells. Moreover, BST2(-/-) mice had lower viral titers in lungs following intranasal infection with vesicular stomatitis virus expressing OVA and influenza B and increased numbers of virus-specific CD8 T cells in the lungs, suggesting that BST2 may facilitate entry and/or replication of enveloped viruses and modulate priming of CD8 T cells. These findings suggest complex roles of BST2 beyond retroviral control in vivo, possibly reflecting the involvement of BST2 in endocytosis and intracellular trafficking of viruses, viral nucleic acids, and Ags.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.1103145