Sökning: id:"swepub:oai:DiVA.org:liu-49962" >
Role of interferon regulatory factor 3 in type I interferon responses in rotavirus-infected dendritic cells and fibroblasts
-
- Douagi, I. (författare)
- Karolinska Institutet
-
- McInerney, G.M. (författare)
- Karolinska Institutet
-
- Hidmark, A.S. (författare)
- Karolinska Institutet
-
visa fler...
-
- Miriallis, V. (författare)
- Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden, Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden
-
- Johansen, K. (författare)
- Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden, Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden
-
- Svensson, Lennart (författare)
- Linköpings universitet,Hälsouniversitetet,Molekylär virologi
-
- Hedestam, G.B.K. (författare)
- Karolinska Institutet
-
visa färre...
-
(creator_code:org_t)
- 2007
- Engelska.
-
Ingår i: Journal of Virology. - 0022-538X .- 1098-5514. ; 81:6, s. 2758-2768
- Relaterad länk:
-
https://urn.kb.se/re...
-
visa fler...
-
https://doi.org/10.1...
-
http://kipublication...
-
visa färre...
Abstract
Ämnesord
Stäng
- 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.
Nyckelord
- MEDICINE
- MEDICIN
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)