Influence of hepatitis B virus infection on intrahepatic natural killer cells and innate lymphoid cell 22 / 临床肝胆病杂志

ABSTRACT

ObjectiveTo investigate the influence of hepatitis B virus (HBV) infection on intrahepatic natural killer (NK) cells and innate lymphoid cell 22 (ILC22), and to provide theoretical and experimental bases for clarifying mechanisms of HBV infection in inducing innate immune response. MethodsA total of 10 male BALC/c aged 6-8 weeks were divided into experimental group and control group, with 5 mice in each group. The mice in the experimental group were treated with the hydrodynamic injection of normal saline containing 10 μg plasmids of complete HBV genome (the volume equaled to 9% of the body weight of the mouse) via the caudal vein, and those in the control group were only treated with normal saline. The mice were scarified 4 days later, and intrahepatic lymphocytes (IHLs) were isolated. Flow cytometry was used to determine the proportions of NK cells and ILC22 subset in IHLs, and the t-test was used for comparison between groups. ResultsHydrodynamic injection of the plasmids containing complete HBV genome induced high levels of HBsAg and HBeAg in mice, with an increase in the serum level of alanine aminotransferase. After HBV infection, the experimental group showed a significant increase in the proportion of intrahepatic NK cells compared with the control group (25.90%±4.92% vs 12.98%±2.13%, t=3.811, P=0.003), while there were no significant differences in the proportions of CD127+ and CD127- NK subsets in NK cells between the two groups. Moreover, after HBV infection, the experimental group showed a significant increase in the proportion of intrahepatic NKp46+ILC22 subset compared with the control group (36.05%±6.85% vs 10.22%±3.54%, t=7.372, P＜0001); however, there was no significant difference in the proportion of NKp46-ILC22 between the two groups. ConclusionHBV infection induces increased levels of intrahepatic NK cells and NKp46+ILC22 cells and thus promotes the innate immune response in the liver.