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The role of γδ T cells in acute hepatitis B virus (HBV) infection remains unclear. For the present study, a mouse model of acute HBV infection was constructed using hydrodynamic injection-based transfection of an HBV DNA plasmid (pHBV). Subsequent changes in the percentages of γδ T cells, expression of activation molecules (CD25 and CD69) and the production of the inflammatory cytokines interferon (IFN)-γ and tumor necrosis factor-α (TNF-α) by liver γδ T cells were investigated using fluorescence-activated cell sorting (FACS). Additionally, the immune responses in the mouse liver were evaluated dynamically by measuring cytokine mRNA expression (IFN-α, IFN-β, IFN-γ or TNF-α) using reverse transcription-quantitative PCR, and other populations of immune cells, including CD4 + T, CD8 + T, natural killer (NK) or natural killer T (NKT) cells, using FACS. On day 1 following acute HBV infection, the percentage of liver γδ T cells was significantly increased along with the high expression of HBV markers. Additionally, liver γδ T cells displayed peak expression of the activation marker CD69 and peak IFN-γ production within this timeframe. IFN-β mRNA expression and the percentage of NK cells were elevated significantly on day 1 in liver tissues. However, there were no significant changes in the spleen or peripheral γδ T cells. Therefore, these data suggested that during the early stages of acute HBV infection, significantly increased numbers of liver γδ T cells may be involved in the enhanced immune response to the increased expression of HBV markers in the liver.

experimental and therapeutic medicine

Increase in liver γδ�T�cells with concurrent augmentation of IFN‑β production during the early stages of a mouse model of acute experimental hepatitis B virus infection