Correlation between toll-like receptor 9 expression in peripheral blood dendritic cells and interferon-α antiviral sustained virological response in patients with chronic hepatitis B

Purpose: To investigate the link between dendritic cells (DC cells), toll-like receptor 9 (TLR9) and tumor necrosis factor-alpha (TFN-alpha) expressions in peripheral blood of patients with chronic hepatitis B (CHB). Methods: Peripheral blood mononuclear cells (PBMC) and CD cells were prepared from CHB patients and healthy volunteers, and the cell proliferation was assessed. The surface expressions of CD83, CD86, CD40 and human leukocyte antigen DR (HLA-DR) on DC cells were assayed by flow cytometry, while the expressions of mRNAs of TLR9, MyD88 and NF-kappa B in each cell-group were determined by fluorescent quantitation PCR. Protein expressions of TLR9, MyD88 and NF-kappa B were analyzed by Western blot. Results: The rate of proliferation of DC cells in the CHB patients was slower than the rate in healthy volunteers (p < 0.05), and the expression of co-stimulatory molecules was significantly lower in CHB patients than in healthy volunteers (p < 0.05). The ability to stimulate T-lymphocyte proliferation of the CHB-DC group was much weaker than that of the D-NC group (p < 0.05). In fluorescent quantitation assays, the relative expressions of mRNAs of TLR9, MyD88 and NF-kappa B in cells of CpG-Stimulate ODN (CpG-S ODN) group were higher than those of the control group (p < 0.05), but the relative expressions of mRNAs of TLR9, MyD88 and NF-kappa B in the cells of the CpG-S ODN group were significantly lower (p < 0.05). Moreover, IFN-alpha level in the CpG-S ODN group was much higher than that in the control group (t = 6.633, p = 0.014 < 0.05). However, results from Western blot showed that the relative expressions of TLR9, MyD88 and NF-kappa B in the CpG-S ODN group were lower than in the control group (p < 0.05). Conclusion: These results indicate that TLR9 on the surface of DC cells of CHB patients can eliminate HBV by generating IFN-alpha via regulation of MyD88 and NF-kappa B.