Study Of The Expression Of IRF3 In Murine Liver Dendritic Cells Intervened By HBV Virions

Objectives:To investigate the molecule immunology mechanism of HBV persistent infection, we observed the expression of IRF3 in murine liver dendritic cells, which were intervened by HBV virions.Methods:The murine liver dendritic cells were isolated via anti-CD11c microbeads, and were incubated with GM-CSF and IL-4 to induce the DCs generation and proliferation. DCs were divided into two groups. One group was cultured with HBV virions in 24h; the other group was cultured without HBV as a normal control group. Then, harvesting the cells and supernatants were detected the expressions of p-IRF3 by western blot and the concentration of IFN-βby ELIS A, after stimulated by poly I:C.Results:1. The expression of IRF3 was too weak to be detected by western blot, before dendritic cells were co-incubation with HBV. The expression of IRF3 was increased after normal dendritic cells were stimulated by poly I:C. The highest expression time-point was between 2h to 6h. The expression of IRF3 was not significantly increased after dendritic cells were incubated with HBV. The ability of expression of IRF3 of DCs was correlated with HBV viral load. High HBV viral load can significantly inhibit expression of IRF3. HBV did not inhibit IRF3 expression significantly, if HBV viral load was lower than 106 copies/ml.2. IFN-βconcentration was 12.38±3.71pg/ml at Oh,88.67±9.01 pg/ml at 6h, 69.89±5.80 pg/ml at 24h in supernatants of HBV group, and was 10.83±4.11 pg/ml at 0h,137.68±12.28 pg/ml at 6h,72.25±8.61 pg/ml at 24h in supernatants of normal control group, respectively. There was no statistically significant difference at 0h(t=0.8398, P>0.05) and at 24h(t=0.6820, P>0.05) between two groups. But, there was statistically significant difference at 6h(t=9.653, P<0.01) between two groups. Conclusion1. The expression of IRF3 was increased after normal dendritic cells were stimulated by poly I:C and had a relationship with different stimulated time-point.2. After co-incubation with HBV, the expression of IRF3 in liver DCs was not increased significantly, compared with normal control. High HBV viral load can inhibit the expression of IRF3 significantly.3. The secretions of IFN-β, downstream of IRF3, were decreased in murine liver dendritic cells after intervened by HBV virions.