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Blockade of Tim-3 Pathway Ameliorates Interferon-γ Production from Hepatic CD8^+ T Cells in a Mouse Model of Hepatitis B Virus Infection 被引量:19

Blockade of Tim-3 Pathway Ameliorates Interferon-γ Production from Hepatic CD8^+ T Cells in a Mouse Model of Hepatitis B Virus Infection
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摘要 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. Cellular & Molecular Immunology. 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. Cellular & Molecular Immunology.
出处 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2009年第1期35-43,共9页 中国免疫学杂志(英文版)
基金 supported in part by grants from the National Nature Science Foundation of China (No. 30670966) the National Basic Research Program (No. 2009CB521900) the Taishan Scholar Program the Scientific Foundation of Innovative Research Team in Shandong University.
关键词 TIM-3 HBV CD8^+ T cell hydrodynamic injection SHRNA Tim-3, HBV, CD8^+ T cell, hydrodynamic injection, shRNA
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