| TLR9 contributes to the recognition of EBV by primary monocytes and plasmacytoid dendritic cells. | |
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MedLine Citation:
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PMID: 20713890 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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TLR9 plays an important role in innate defense against viruses by the detection of CpG motifs of foreign DNA within intracellular compartments. In this study, we evaluated the ability of EBV to promote monocyte and plasmacytoid dendritic cell (pDC) activation and cytokine release through TLR9 activation. We demonstrated that treatment of primary monocytes with EBV and with purified EBV DNA induced the release of IL-8 through TLR9. Activation of TLR9 by viral DNA requires endosomal maturation because pretreatment of monocytes with chloroquine strongly reduced IL-8 secretion. However, pretreatment of monocytes with siRNA directed against TLR2, with inhibitory ODN (iODN) or with a combination of both inhibitors strongly reduced the secretion of IL-8, providing evidence of a dual action of TLR2 and TLR9 in EBV recognition by monocytes. In contrast, production of MCP-1 and IL-10 in EBV-treated monocytes was mainly regulated through TLR2. Although EBV does not establish infection in pDCs, challenge with either live EBV particles or isolated EBV DNA was found to induce the release of IFN-alpha through TLR9, as supported by blockage of TLR9 activity with iODN or chloroquine. The role of TLR9 in the recognition of EBV by pDCs appears to be dominant, as confirmed by the marked inhibitory effect of iODN observed on the synthesis of IFN-alpha, IL-6, and IL-8 by pDCs. These results demonstrate that recognition of EBV by TLR9 is differently orchestrated in primary monocytes and pDCs to optimize viral recognition and antiviral response. |
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Authors:
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Stéphanie Fiola; David Gosselin; Kenzo Takada; Jean Gosselin |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-08-16 |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 185 ISSN: 1550-6606 ISO Abbreviation: J. Immunol. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-09-03 Completed Date: 2010-11-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 3620-31 Citation Subset: AIM; IM |
Affiliation:
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Laboratory of Innate Immunology, Centre Hospitalier Universitaire de Québec Research Center, Québec City, Québec, Canada. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Cell Communication
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genetics,
immunology Cells, Cultured Cytokines / biosynthesis Dendritic Cells / immunology*, metabolism, virology* Epstein-Barr Virus Infections / immunology, metabolism, pathology Gene Expression Regulation / immunology Herpesvirus 4, Human / immunology*, pathogenicity Humans Inflammation Mediators / physiology Monocytes / immunology*, metabolism, virology* Protein Transport / genetics, immunology Toll-Like Receptor 9 / biosynthesis, genetics, physiology* Up-Regulation / genetics, immunology |
| Grant Support | |
ID/Acronym/Agency:
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//Canadian Institutes of Health Research |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Inflammation Mediators; 0/TLR9 protein, human; 0/Toll-Like Receptor 9 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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