Tick salivary cystatin sialostatin L2 suppresses IFN responses in mouse dendritic cells
Language English Country England, Great Britain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
25408129
DOI
10.1111/pim.12162
Knihovny.cz E-resources
- Keywords
- cystatin, dendritic cell, interferon, tick,
- 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
- Names of Substances
- Cystatins MeSH
- Interferon-beta MeSH
- Interferon Regulatory Factor-7 MeSH
- IP10-Mig receptor MeSH Browser
- Irf7 protein, mouse MeSH Browser
- Lipopolysaccharides MeSH
- Receptors, Cytokine MeSH
- Receptors, Interferon MeSH
- sialostatin L, Ixodes scapularis MeSH Browser
- Salivary Cystatins 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.
References provided by Crossref.org
Insights into the Role of Tick Salivary Protease Inhibitors during Ectoparasite-Host Crosstalk
Tick Salivary Compounds for Targeted Immunomodulatory Therapy
The Use of Tick Salivary Proteins as Novel Therapeutics
Salivary Tick Cystatin OmC2 Targets Lysosomal Cathepsins S and C in Human Dendritic Cells
For Whom the Bell Tolls (and Nods): Spit-acular Saliva
All For One and One For All on the Tick-Host Battlefield
Tick sialostatins L and L2 differentially influence dendritic cell responses to Borrelia spirochetes
