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Role of interferon regulatory factor 3 in type I interferon responses in rotavirus-infected dendritic cells and fibroblasts
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden, Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden.
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden, Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden.
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden, Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden.
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2007 (English)In: Journal of Virology, ISSN 0022-538X, E-ISSN 1098-5514, Vol. 81, no 6, 2758-2768 p.Article in journal (Refereed) Published
Abstract [en]

The main pathway for the induction of type I interferons (IFN) by viruses is through the recognition of viral RNA by cytosolic receptors and the subsequent activation of interferon regulatory factor 3 (IRF-3), which drives IFN-a/ß transcription. In addition to their role in inducing an antiviral state, type I IFN also play a role in modulating adaptive immune responses, in part via their effects on dendritic cells (DCs). Many viruses have evolved mechanisms to interfere with type I IFN induction, and one recently reported strategy for achieving this is by targeting IRF-3 for degradation, as shown for rotavirus nonstructural protein 1 (NSP1). It was therefore of interest to investigate whether rotavirus-exposed DCs would produce type I IFN and/or mature in response to the virus. Our results demonstrate that IRF-3 was rapidly degraded in rotavirus-infected mouse embryonic fibroblasts (MEFs) and type I IFN was not detected in these cultures. In contrast, rotavirus induced type I IFN production in myeloid DCs (mDCs), resulting in their activation. Type I IFN induction in response to rotavirus was reduced in mDCs from IRF-3-/- mice, indicating that IRF-3 was important for mediating the response. Exposure of mDCs to UV-treated rotavirus induced significantly higher type I IFN levels, suggesting that rotavirus-encoded functions also antagonized the response in DCs. However, in contrast to MEFs, this action was not sufficient to completely abrogate type I IFN induction, consistent with a role for DCs as sentinels for virus infection. Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Place, publisher, year, edition, pages
2007. Vol. 81, no 6, 2758-2768 p.
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Medical and Health Sciences
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URN: urn:nbn:se:liu:diva-49962DOI: 10.1128/JVI.01555-06OAI: oai:DiVA.org:liu-49962DiVA: diva2:270858
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2017-12-12

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Svensson, Lennart

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