自噬
HBcAg
生物
乙型肝炎表面抗原
病毒学
细胞毒性T细胞
CTL公司*
乙型肝炎病毒
CD8型
抗原
免疫学
病毒
细胞凋亡
体外
遗传学
作者
Quanhui Tan,Chen Jie,Gao Gao,YiZhang,Xiaohua Chen,Yongsheng Yu,Zang Guo-qin,Zhenghao Tang
摘要
Early studies have shown that autophagy and TPPII are associated with HBV infection. In this study, adenovirus vector containing TPPII was constructed to immunize HBV transgenic mice in vivo to explore the potential mechanism of autophagy and HBV infection. Our goal is to provide new ideas for immunotherapy of hepatitis B. First, adenovirus vector containing TPPII was constructed. Then, we used adenovirus to immunize HBV transgenic mice and ATG5 knockout HBV transgenic mice. The autophagy of CD8+ T cells was detected by transmission electron microscopy and immunofluorescence electron microscopy, Western blot was used to detect the expression of autophagy LC3 and BECN1, CTL reaction, HBV DNA and HBsAg in serum, HBsAg and HBcAg in liver tissues by immunohistochemistry, to further examine the possible mechanisms involved in autophagy. Adv-HBcAg-TPPII promotes autophagy of CD8+ T lymphocyte, activates CTL response, inhibits HBV DNA replication and HBsAg expression, and PI3K/ Akt /m TOR signalling pathway may be involved in autophagy. This study demonstrates that autophagy of CD8+ T cells was induced by Adv-HBcAg-TPPII and the molecular mechanism may be related to the PI3K/ Akt /m TOR signalling pathway, providing a possible theoretical basis for immunotherapy of hepatitis B.
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