血吸虫病严重危害人类健康，肝脏虫卵肉芽肿及其纤维化是该病主要病理变化，是晚期患者死亡的主要原因。γδT细胞是IL-17的重要来源，在炎症和免疫稳态中发挥重要功能。我们前期研究发现日本血吸虫感染小鼠肝脏虫卵肉芽肿γδT细胞分布与中性粒细胞相似，阻断IL-17的重要来源细胞Vγ2亚型γδT细胞能减轻纤维化程度，降低中性粒细胞比例和IL-17含量。提示Vγ2 γδT细胞可能在促进肝纤维化中发挥重要作用。本项目拟采用日本血吸虫感染小鼠模型，运用流式细胞术、免疫组化、转录组分析和基因敲除小鼠细胞过继转输等免疫学与分子生物学技术，重点关注在日本血吸虫感染进程中，Vγ2 γδT细胞招募中性粒细胞促进肝纤维化的作用及其机制。本项目预期结果将为阐明日本血吸虫感染复杂的致病机制研究提供新视角，对开展临床相关治疗研究提供科学依据和分子基础。

As main pathological features of schsitosomiasis, egg granulomas and fibrosis are a leading cause of death in late patients, so schistosomiasis remains a serious threat to human health. As an important source of IL-17, γδT cells play an important role in inflmmation and immune homeostasis. We found that γδT cells have similar distribution with neutrophils in liver granuloma of Schistosoma japonicum infected mice. Vγ2 γδT cells , an important source of IL-17, are blocked resulting in reducing fibrosis following the reduction of the proportion of neutrophils and the content of IL-17. It suggested that Vγ2 γδT cells may play an important role in promoting liver fibrosis. The project aims to adopt the mouse model of S. japonicum infection, using immunology and molecular biology techniques including flow cytometry, immunohistochemistry, transcriptome analysis, and adoptive transfer of cells into gene knockout mice, and focus on the mechanism for Vγ2 γδT cells recruit neutrophils to promote liver fibrosis in the process of S. japonicum infection. The expected results of this project will provide a new perspective for elucidating complicated pathogenic mechanism of S. japonicum infection, and provide a scientific basis for research and molecular basis of clinical treatment.