HBV transinfected enhances the PD-L expression of cytokines stimulating / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To investigate whether the PD-L expression in the liver cell lines transinfected with HBV (HepG2.2.15 cells) can be up-regulated after cytokines stimulating.</p><p><b>METHODS</b>To apply the liver cell lines (HepG2 cells and HepG2.2.15 cells) as a model, the cells were stimulated with IL-4, IFN-alpha and IFN-gamma (final concentration were 10 ng/ml, stimulated for 12 hours) and RT-PCR was carried out to determine the PD-L expression before and after cytokines stimulating.</p><p><b>RESULTS</b>Whether or not transinfected with HBV, IFN-alpha and IFN-gamma both can induce the liver cell lines (HepG2 cells and HepG2.2.15 cells) PD-L1 expression while IL-4 can not; IL-4, IFN-alpha, IFN-gamma all can induce the PD-L2 expression in HepG2.2.15 cells which was transinfected with HBV, only IFN-gamma can induce the PD-L2 expression in HepG2 cells which was not transinfected with HBV.</p><p><b>CONCLUSION</b>IFN-alpha, IFN-gamma both can induce the PD-L1 expression in HepG2 cells and HepG2.2.15 cells, while it is easy for cytokines to induce the PD-L2 expression in HepG2.2.15 cells which was transinfected with HBV, this may provide a potential mechanism of the molecular basis for chronic HBV infection.</p>

Association of genetic polymorphisms in glutathione S-transferases M1 with hepatitis beta-related hepatocellular carcinoma / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the association of genetic polymorphisms in glutathione S-transferases(GST) M1 with hepatitis beta-related hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>Genomic DNA was isolated from peripheral blood of HBsAg carriers, including 91 cases of HCC, 58 liver cirrhosis(LC), 63 chronic hepatitis B(CHB), and 134 normal controls. GSTM1 genotypes were detected by multiplex PCR.</p><p><b>RESULTS</b>The null genotype of GSTM1 was significantly frequent in patients with HCC compared with controls (P<0.05), but there were no significant differences in frequency of GSTM1 null genotype among patients with liver cirrhosis, chronic hepatitis B and normal controls. Subjects carrying null genotypes of GSTM1 had higher risk of developing HCC compared with those carrying positive genotype (OR=1.81.95% CI=1.05 approximately equals 3.12).</p><p><b>CONCLUSION</b>The GSTM1-null genotype may be associated with an increased risk of HCC, but not of CHB and LC.</p>