Abstract
The antigen recognition and immune response to acute and chronic hepatitis B virus (HBV) infections are the result of both the innate and adaptive immune response. The innate immune response comprises Dendritic Cells (DCs), which served as professional antigen-presenting cells and a bridge between innate and adaptive immunity, Kupffer cells and inflammatory monocytes for the continuous inflammation of hepatocyte, neutrophils for hepatic tissue damage due to acute inflammation, type I interferons (IFN), which induce an antiviral state on infected cells, directs natural killer (NK) cells to kill virally infected cells, reduces the population of infected cells, and promotes the effective maturation and site recruitment of adaptive immunity through the production of pro-inflammatory cytokines and chemokines. Through stimulating B cells, T-helper, and cytotoxic T cells, the adaptive immune system also protects against hepatitis B infection. During HBV infection, a network of cell types that can either play protective or harmful functions creates the anti-viral adaptive immune response. These many elements, such as Cluster of differentiation four (CD4) T cells (traditionally known as helper T cells), are potent cytokine producers and necessary for the effective maturation of effector cytotoxic cluster of differentiation eight (CD8) T cells and B cell antibody production. By cytolytic and non-cytolytic processes, CD8 T cells are able to eliminate HBV-infected hepatocytes and directly detect virus-infected cells, and circulating CD4+ CD25+ regulatory T cells for the modulation of immune system. In order to avoid reinfection, B cells can produce antibodies that destroy free viral particles. Moreover, by presenting HBV antigens to helper T cells, B cells may also influence how well these cells operate.