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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,
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Free Medical Journals
od 1997 do Před 1 rokem
Medline Complete (EBSCOhost)
od 1998-01-01 do Před 1 rokem
Wiley Free Content
od 1997 do Před 1 rokem
PubMed
25408129
DOI
10.1111/pim.12162
Knihovny.cz E-zdroje
- MeSH
- Borrelia burgdorferi fyziologie MeSH
- cystatiny imunologie MeSH
- dendritické buňky imunologie MeSH
- fosforylace MeSH
- interferon beta imunologie MeSH
- interferonový regulační faktor 7 imunologie MeSH
- klíště imunologie mikrobiologie MeSH
- lipopolysacharidy imunologie MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- receptory cytokinové imunologie MeSH
- receptory interferonů metabolismus MeSH
- slinné cystatiny imunologie MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem 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.
Citace poskytuje Crossref.org
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