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Tick salivary cystatin sialostatin L2 suppresses IFN responses in mouse dendritic cells
J. Lieskovská, J. Páleníková, J. Širmarová, J. Elsterová, M. Kotsyfakis, A. Campos Chagas, E. Calvo, D. Růžek, J. Kopecký,
Language English Country England, Great Britain
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 1997 to 1 year ago
Medline Complete (EBSCOhost)
from 1998-01-01 to 1 year ago
Wiley Free Content
from 1997 to 1 year ago
PubMed
25408129
DOI
10.1111/pim.12162
Knihovny.cz E-resources
- MeSH
- Borrelia burgdorferi physiology MeSH
- Cystatins immunology MeSH
- Dendritic Cells immunology MeSH
- Phosphorylation MeSH
- Interferon-beta immunology MeSH
- Interferon Regulatory Factor-7 immunology MeSH
- Ixodes immunology microbiology MeSH
- Lipopolysaccharides immunology MeSH
- Mice, Inbred C57BL MeSH
- Mice MeSH
- Receptors, Cytokine immunology MeSH
- Receptors, Interferon metabolism MeSH
- Salivary Cystatins immunology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
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.
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