肝泡型包虫病亦称“虫癌”是由泡状棘球蚴绦虫（E.m）感染所致的严重危害百姓健康的人畜共患病。肝切除和自体肝移植仍是根治措施。术后肝功不全是影响手术成功的关键因素。我们系列研究结果提示，肝泡型包虫病患者和E.m感染小鼠健侧肝明显再生，提示可能和E.m感染对宿主Kupffer细胞的调节和介导炎性因子IL-6表达有关。但其具体途径和可能的区域分子免疫机制未知。本研究计划利用人体组织标本和动物模型，通过流式技术，基因敲除鼠，Western Blot，免疫组化等技术，从体内外实验体系和临床患者等多个水平，了解感染状态下Kupffer细胞成熟分化和抗原呈递功能变化，继而解析E.m驯化的Kupffer 细胞对肝再生的影响，并最终在E.m/TLR4/MyD88/NF-κB/STAT3/IL-6信号转导途径免疫应答轴中发现关键作用因子，为阐明肝泡型包虫所致肝再生的区域分子免疫机制和预防肝功不全提供理论依据。

Hepatic alveolar echinococcosis (HAE), also known as “parasitic cancer”, is caused by the larval stage of the tapeworm Echinococcus multilocularis (E.m) and still imposes great threat on health. Radical hepatic resection and liver auto-transplantation are priority. However, post-operative liver dysfunction is a major obstacle for surgical success. A series of previous works of us have revealed an obvious liver regeneration in HAE patients and E.m infected murine model and postulated a correlation between the immune regulation on host’s Kupffer cells and the secretion of inflammatory cytokine IL-6. Nonetheless, the possible pathways and molecular mechanism are still remained unknown. This research aims at the immunological role of TLR4/MyD88/NF-kB pathway and its possible mechanism in liver regeneration caused by E.m infection by using flow cytometry, Western-Blot, immunohistochemistry and gene knockout mice, further find out the key cytokine and molecules that may play significant role in the regulation of liver regeneration. In addition, the possible mechanism of E.m/TLR4/MyD88/NF-kB/STAT3/IL-6 signal transduction pathway during liver regeneration caused by E.m infection will be studied. This study may provide theoretical support for immunological mechanism and to prevent the post-operative liver dysfunction during E.m infection.