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/

Global: Zendy Plus annual

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

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Plasmacytoid dendritic cells (pDCs) were treated with cytosine-phosphate-guanine (CpG) DNA, and cell apoptosis, signals and immune responses were measured to investigate the effects and mechanism of CpG DNA in pDCs from chronic hepatitis B patients. CpG DNA-stimulated pDCs secreted more IFN-α than the control pDCs. CpG DNA activated Toll-like receptor 9 (TLR9), thereby resulting in the upregulated expression of myeloid differentiation primary response gene 88 (MyD88), interferon regulatory factor 7 (IRF7) and nuclear factor kappa B (NF-κB). Furthermore, CpG DNA down-regulated apoptosis and promoted the expression of IFN-α, interleukin-12 (IL-12), IL-21, IL-26 and tumour necrosis factor-α (TNF-α) in pDCs. Following treatment with NF-κB inhibitor, pyrollidine dithiocarbamate (PDTC), the influence of CpG DNA on pDCs was inhibited. Our results suggest that CpG DNA may directly interfere with the function of pDCs through TLR9-mediated upregulation of MyD88, IRF7 and NF-κB expression, which can partially explain the activation of pDCs in chronic hepatitis B patients.

archives of physiology and biochemistry

CpG DNA-triggered upregulation of TLR9 expression affects apoptosis and immune responses in human plasmacytoid dendritic cells isolated from chronic hepatitis B patients