NK Cells Involve In Elimination Of HBV

Background and Objective Recently,Scientists have recognized that the liver can be regarded as as a major organ which has the innate immune system.The liver lymphocyte population is enriched in innate immune cells,such as macrophage,NK cells and NKT cells.HBV can infect human liver and establish chronic disease in the liver.In our study,we want to investigate the mechanism of NK cell in eliminating the HBV during acute infection.Methods Adult mice hydrodynamically injected with 20?g of p GEM4Z/HBV1.2plasmid were used to establish the acute HBV infection model.This model was evaluated by detecting serum level of HBs Ag and HBc Ag in liver tissue at the indicated time points by radioimmunoassay and immunohistochemistry respectively.The variation of frequency and absolute number of NK cell was analyzed between wide type(WT)mice and HBV plasmid-injected mice.Furthermore,the activation and the capacity to produce IFN-? of NK cell were investigated in these mice by flow cytometry.Liver injury was observed with the use of HE staining and alanine transaminase(ALT)dectection.To test whether NK cell and IFN-? secreted by it involved in HBV elimination,we used PK136 antibody to clear NK cell and IFN-?neutralization antibody to block IFN-? effect.Results After the hydrodynamic injection with 20?g of pGEM4Z/HBV1.2,the serum level of HBs Ag and expression of HBc Ag in liver tissue were very high at time point of 1 week,but then decreased obviously.However,these antigens almost became negative at 4-5 weeks,which mimic acute HBV infection patients.Compared with NK cell from control mice,the proportion and absolute number of NK cell increased significantly from HBV mice.Also,the NK cells express higher level of CD69 and produce more IFN-?.Meanwhile,there was no any injury in liver of HBV mice.Depletion of NK cell or blocking IFN-? effect in HBV mice result in the increased level of HBV related antigens.Conclusion In the mouse model of acute HBV infection,NK cell could promote the HBV elimination through secreting IFN-?.