English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

Plasmacytoid dendritic cells (pDCs) are responsible for the production of type I IFN during viral infection. Viral elimination by IFN-alpha-based therapy in more than 50% of patients chronically infected with hepatitis C virus (HCV) suggests a possible impairment of production of endogenous IFN-alpha by pDCs in infected individuals. Recent studies in the HCVcc-exposed pDCs purified from healthy donors show that HCV is a weak inducer of IFN-alpha in vitro and that HCVcc blocks the TLR9mediated IFN-alpha production. It has been also reported that PI3K/AKT is critical for type I IFN production by pDCs in response to TLR agonists. The specific aim of the present study is to investigate the effect of HCV on PI3K/AKT signaling. Methods To this end we exposed pDCs from healthy donors to insect cell-derived HCV-like particles (HCV-LP) or an insect cell control preparation in the presence or absence of TLR7 and TLR9 agonists and determined dynamics of PI3K/AKT phosphorylation by flow cytometry. By this approach we compared the early (AKT phosphorylation) and late (IFN-alpha production) steps of TLR7/TLR9-MyD88 signaling. The levels of cell-free supernatant-secreted IFN-alpha were determined by ELISA.

Highjacking of PI3K/AKT signaling pathway by Hepatitis C virus in TLR9-activated human plasmacytoid dendritic cells