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Tick salivary cystatin sialostatin L2 suppresses IFN responses in mouse dendritic cells.
- Source :
- Parasite Immunology; Feb2015, Vol. 37 Issue 2, p70-78, 10p
- Publication Year :
- 2015
-
Abstract
- Type I interferon ( IFN), mainly produced by dendritic cells ( DCs), is critical in the host defence against tick-transmitted pathogens. Here, we report that salivary cysteine protease inhibitor from the hard tick Ixodes scapularis, sialostatin L2, affects IFN-β mediated immune reactions in mouse dendritic cells. Following IFN receptor ligation, the Janus activated kinases/signal transducer and activator of transcription ( JAK/ STAT) pathway is activated. We show that sialostatin L2 attenuates phosphorylation of STATs in spleen dendritic cells upon addition of recombinant IFN-β. LPS-stimulated dendritic cells release IFN-β which in turn leads to the induction of IFN-stimulated genes ( ISG) through JAK/ STAT pathway activation. The induction of two ISG, interferon regulatory factor 7 ( IRF-7) and IP-10, was suppressed by sialostatin L2 in LPS-stimulated dendritic cells. Finally, the interference of sialostatin L2 with IFN action led to the enhanced replication of tick-borne encephalitis virus in DC. In summary, we present here that tick salivary cystatin negatively affects IFN-β responses which may consequently increase the pathogen load after transmission via tick saliva. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 01419838
- Volume :
- 37
- Issue :
- 2
- Database :
- Complementary Index
- Journal :
- Parasite Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 100549561
- Full Text :
- https://doi.org/10.1111/pim.12162