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- W2116301291 abstract "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-alpha/beta 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." @default.
- W2116301291 created "2016-06-24" @default.
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- W2116301291 creator A5089160183 @default.
- W2116301291 date "2007-03-15" @default.
- W2116301291 modified "2023-10-01" @default.
- W2116301291 title "Role of Interferon Regulatory Factor 3 in Type I Interferon Responses in Rotavirus-Infected Dendritic Cells and Fibroblasts" @default.
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- W2116301291 doi "https://doi.org/10.1128/jvi.01555-06" @default.
- W2116301291 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1865971" @default.
- W2116301291 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17215281" @default.
- W2116301291 hasPublicationYear "2007" @default.
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