Abstract

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.

摘要

用胞嘧啶-磷酸-鸟嘌呤（CpG）DNA处理浆细胞样树突状细胞（pDC），并测量细胞凋亡，信号和免疫应答，以研究CpG DNA在慢性乙型肝炎患者的pDC中的作用和机制。CpG DNA刺激的pDC比对照pDC分泌更多的IFN-α。CpG DNA激活了Toll样受体9（TLR9），从而导致了髓样分化初级应答基因88（MyD88），干扰素调节因子7（IRF7）和核因子κB（NF-κB）的表达上调。此外，CpG DNA下调了细胞凋亡，并促进了pDC中IFN-α，白介素12（IL-12），IL-21，IL-26和肿瘤坏死因子-α（TNF-α）的表达。用NF-κB抑制剂吡咯烷二硫代氨基甲酸酯（PDTC）处理后，CpG DNA对pDC的影响被抑制。