期刊
PARASITE IMMUNOLOGY
卷 37, 期 2, 页码 70-78出版社
WILEY-BLACKWELL
DOI: 10.1111/pim.12162
关键词
tick; dendritic cell; interferon; cystatin
资金
- Czech Science Foundation [P302/12/2208, 14-25799S]
- MEYS of the Czech Republic under the NPU I program [LO1218]
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- 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-. LPS-stimulated dendritic cells release IFN- 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- responses which may consequently increase the pathogen load after transmission via tick saliva.
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