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T cell immunoglobulin-and mucin-domain-containing molecule-3(Tim-3) has been reported to participate in the pathogenesis of inflammatory diseases. However,whether Tim-3 is involved in hepatitis B virus(HBV) infection remains unknown. Here,we studied the expression and function of Tim-3 in a hydrodynamics-based mouse model of HBV infection. A significant increase of Tim-3 expression on hepatic T lymphocytes,especially on CD8+ T cells,was demonstrated in HBV model mice from day 7 to day 18. After Tim-3 knockdown by specific shRNAs,significantly increased IFN-γ production from hepatic CD8+ T cells in HBV model mice was observed. Very interestingly,we found Tim-3 expression on CD8+ T cells was higher in HBV model mice with higher serum anti-HBs production. Moreover,Tim-3 knockdown influenced anti-HBs production in vivo. Collectively,our data suggested that Tim-3 might act as a potent regulator of antiviral T-cell responses in HBV infection.
T cell immunoglobulin-and mucin-domain-containing molecule-3 (Tim-3) has been reported to participate in the pathogenesis of inflammatory diseases. However, whether Tim-3 is involved in hepatitis B virus (HBV) infection remains unknown. Here , we studied the expression and function of Tim-3 in a hydrodynamics-based mouse model of HBV infection. A significant increase of Tim-3 expression on hepatic T lymphocytes, especially on CD8 + T cells, was demonstrated in HBV model mice from day 7 to day 18. Very interestingly, we found that Tim-3 expression on CD8 + T cells was higher in HBV model mice we suggest that Tim-3 knockdown influenced anti-HBs production in vivo. Collectively, our data suggested that Tim-3 might act as a potent regulator of antiviral T-cell responses in HBV infection.