Tick salivary cystatin sialostatin L2 suppresses IFN responses in mouse dendritic cells.

Autor: Lieskovská, J., Páleníková, J., Širmarová, J., Elsterová, J., Kotsyfakis, M., Campos Chagas, A., Calvo, E., Růžek, D., Kopecký, J.
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Zdroj: Parasite Immunology; Feb2015, Vol. 37 Issue 2, p70-78, 10p
Abstrakt: 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]
Databáze: Complementary Index
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