Tick saliva suppresses IFN signalling in dendritic cells upon Borrelia afzelii infection
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Borrelia burgdorferi Group pathogenicity MeSH
- Dendritic Cells immunology MeSH
- Immunologic Factors immunology metabolism MeSH
- Interferon Type I antagonists & inhibitors immunology MeSH
- Ixodes immunology MeSH
- Cells, Cultured MeSH
- Mice, Inbred C57BL MeSH
- Mice MeSH
- Saliva immunology metabolism 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
- Immunologic Factors MeSH
- Interferon Type I MeSH
Type I interferons (IFN-α and IFN-β) are crucial determinants of the host immune response and tick saliva modulates this response, thus facilitating the transmission of tickborne pathogens. The current study therefore examines the effect of Ixodes ricinus tick saliva on IFN-β signalling in murine dendritic cells using lipopolysaccharide (LPS) and Borrelia afzelii spirochaetes as inducers. Activated dendritic cells secret IFN that activates Signal Transducer and Activator of Transcription 1 (STAT-1). Our results show that Borrelia-induced activation of STAT-1 was suppressed by tick saliva. As the amount of secreted IFN-β was not influenced by tick saliva, the results indicated that saliva affected the interferon pathway at the IFN receptor or downstream of it. By using recombinant IFN-β, we show that tick saliva attenuates IFN-triggered STAT-1 activation. Tick saliva also inhibited LPS-induced IFN-β production suggesting that saliva interferes with the activation of the pathway that mediates IFN-β induction. Our data indicate that I. ricinus tick saliva may modulate the host immune response by attenuating the initial signal transduction pathway of type I IFN.
References provided by Crossref.org
Modulation of host immunity by tick saliva