Exosomes loading Tapasin enhance T cell immune response by autophagy to inhibit HBV replication

免疫系统 T细胞 生物 细胞毒性T细胞 获得性免疫系统 CD8型 自噬 乙型肝炎病毒 病毒学 细胞生物学 免疫学 病毒 体外 细胞凋亡 生物化学
作者
Mengjiao Lv,Ting Yao,Yi Zhang,Siyuan Ma,Jinmei Chen,Zhenghao Tang,Guoqing Zang,Xiaohua Chen
出处
期刊:Journal of Medical Virology [Wiley]
卷期号:95 (4) 被引量:2
标识
DOI:10.1002/jmv.28746
摘要

Hepatitis B virus (HBV) specific T cell immune response plays a vital role in viral clearance. Dendritic cell derived exosomes (Dexs) can activate T cell immunity effectively. Tapasin (TPN) is involved in antigen processing and specific immune recognition. In the present study, we elucidated that Dexs loading TPN (TPN-Dexs) could enhance CD8+ T cell immune response and inhibit virus replication in HBV transgenic mice. T cell immune response and the ability of inhibiting HBV replication were measured in HBV transgenic mice immunized with TPN-Dexs. Meanwhile, CD8+ T cell autophagy and specific T cell immune responses were measured in vitro and vivo, and the mechanisms probably involved in were explored. Purified TPN-Dexs could be taken up into the cytoplasm of DCs and upregulate CD8+ T cell autophagy to enhance specific T cell immune response. In addition, TPN-Dexs could increase the expression of AKT and decrease the expression of mTOR in CD8+ T cells. Further research confirmed that TPN-Dexs could inhibit virus replication and decrease the expression of HBsAg in the liver of HBV transgenic mice. Nevertheless, those also could elicit mice hepatocytes damage. In conclusion, TPN-Dexs could enhance specific CD8+ T cell immune responses via the AKT/mTOR pathway to regulate the autophagy and exert the antiviral effect in HBV transgenic mice.
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