巨噬细胞M2型极化在日本血吸虫病肉芽肿形成和组织修复过程中发挥着重要作用，但髓系细胞触发受体-2(TREM-2)是否调控其巨噬细胞M2型极化尚未清楚。本项目前期实验结果显示在日本血吸虫感染中随着巨噬细胞M1型优势向M2型优势偏移，巨噬细胞上TREM-2表达相应增加；SEA可诱导TREM-2表达上调。据此推测：SEA可能通过某种或某些信号通路上调TREM-2，诱导巨噬细胞向M2型极化。为了探明其机制，本项目将运用Trem-2-/-小鼠血吸虫病模型和巨噬细胞株，通过流式细胞术、RT-qPCR、Western blotting、免疫荧光、CRISPR-Cas9技术、RNA干扰、ChIP、EMSA等技术深入探讨TREM-2在SEA诱导巨噬细胞M2型极化中的作用及分子机制。预期结果将深化对日本血吸虫感染引起的巨噬细胞M2型极化成因的认识，为日本血吸虫病肝纤维化防治提供新的潜在靶点。

The polarization of alternatively activated macrophages (M2 macrophages) is critical for granuloma formation and tissue repair of schistosomiasis japonicum. However, it remains unclear whether triggering receptor-2 expressed on myeloid cells (TREM-2) is implicated in regulating M2 polarization of macrophages during the infection of Schistosoma japonicum. In our previous study, we found that macrophages were typically skewed from M1 towards the M2 polarization, accompanied with the enhanced expression of TREM-2 in macrophages during Schistosoma japonicum infection. Moreover, the soluble egg antigens induced the upregulation of the expression of TREM-2 in vitro. It is speculated that the soluble egg antigens may upregulate TREM-2, and thereby induce M2 polarization via one or some signal pathways. In order to explore its role and the underlying mechanism, Trem-2-/- mouse model of schistosomiasis and macrophages lines are used. We also study the role and the underlying mechanism of TREM-2 on soluble egg antigens-induced M2 polarization of macrophages by Flow cytometry, reverse transcriptase (RT)-qPCR, Western blotting, Immunofluorescence, CRISPR/Cas9, RNA interference, ChIP, EMSA and so on. Desired outcomes not only go step further to deepen the understanding of the cause of M2 polarization of macrophages, but also provide the potential target that could prevent liver fibrosis in schistosomiasis japonicum.