布鲁氏菌病是新疆地区严重的人畜共患病，对其发病机制认识不足阻碍了有效的防治研究。Tim-3/Galectin-9在病原体的免疫逃避中发挥了重要作用，但其在布鲁氏菌病中的作用尚未明确。我们前期发现，Tim-3/Galectin-9也参与了布鲁氏菌的免疫逃避，但其机制尚不清楚。本项目从布鲁氏菌病患者和感染小鼠Tim-3/Galectin-9分子介导的免疫逃避为切入点，研究治疗前后布鲁氏菌病患者和感染小鼠Tim-3/Galectin-9通路的激活，明确其与布鲁氏菌病关系。通过阻断Tim-3/Galectin-9通路，分析Tim-3/Galectin-9通路对巨噬细胞和T细胞功能活性的负调控作用，阐明宿主免疫抑制状态形成和维持上所起的作用。用野生布鲁氏菌调节Tim-3/Galectin-9通路对巨噬细胞和T细胞影响，阐明布鲁氏菌感染与宿主免疫的关系，为开展以阻断免疫逃避信号途径为靶点的布鲁斯菌病防

Brucellosis is a serious zoonosis in Xinjiang. The lack of knowledge of the pathogenesis of brucellosis hinders the effective prevention and control. Tim-3/Galectin-9 plays an important role in the immune evasion of pathogens. But its role in brucellosis is not clear. Our Preview study show that Tim-3/Galectin-9 was involved in the immune evasion of Brucella. However, the mechanism is not clear. Based on the immune evasion mediated by Tim-3/Galectin-9 molecule in brucellosis patients and infected mice, the activation of Tim-3/Galectin-9 pathway in brucellosis patients and infected mice before and after treatment was studied, in order to clarified the relationship between Tim-3/Galectin-9 pathway and brucellosis. we analyze the the negative regulatory effect of Tim-3/Galectin-9 pathway on the functional activity of macrophages and T cells by blocking the Tim-3/Galectin-9 pathway， to elucidate the role of host immunosuppressive state formation and maintenance, Regulation of Tim-3/Galectin-9 Pathway by Wild Brucella on macrophages and T cells were studied in order to clarified the relationship between brucella infection and host immunity, which provided a new idea for the study of the prevention and treatment of Bruce's disease, which was aimed at blocking immune escape signal pathway.