免疫抑制所致的严重感染以及多器官功能损伤是脓毒症患者死亡的重要因素之一，肝脏作为重要的免疫调控器官，其功能损伤是导致脓毒症患者死亡的独立危险因素之一。CD8+T细胞是机体重要的免疫细胞，其功能缺陷或耗竭是脓毒症患者容易“二次感染”的关键因素之一。目前脓毒症中CD8+T细胞功能损伤机制并不明确。Tim-3/Galectin-9共抑制信号通路调控多种免疫细胞的功能，参与脓毒症所致的免疫耐受。本课题以脓毒症小鼠模型为研究对象，研究 Tim-3/Galectin-9分子在脓毒症中表达特点，以及其参与诱导肝内CD8+T细胞功能耗竭及肝脏免疫耐受作用及其机制。本项目将有助于进一步阐明Tim-3/Galectin-9共抑制信号通路在脓毒症中诱导CD8+T细胞功能耗竭及肝脏免疫耐受的机制，为探索更有效阻断脓毒症所致免疫耐受策略提供理论基础和实验依据。

Severe infection and multiple organ damage caused by immunosuppression are key factors in the death of patients with sepsis. The liver works as a lymphoid organ in response to sepsis. Liver dysfunction after sepsis is an independent risk factor for multiple organ dysfunction and sepsis-induced death. As an important immune cell, the function defects or exhaustion of CD8+ T cells are key factors that patients susceptible to "secondary infection" in sepsis. The mechanism of functional impairment of CD8+T cells is still not clear at the end of sepsis. The function of multiple immune cells are regulated by the Tim-3/Galectin-9 co-inhibitory pathway, which also participates in the immune tolerance induced by sepsis. In this study, septic mouse model will be used to investigate the expression characteristic of Tim-3/Galectin-9 pathway in sepsis. The function and mechanism of Tim-3/Galectin-9 pathway in inducing hepatic CD8+T cells exhaustion and liver immune tolerance will be investigated. Our research will further elucidate the mechanism of Tim-3/Galectin-9 co-inhibitory pathway in inducing the CD8+T cells exhaustion and liver immune tolerance in sepsis, and provide more theoretical and experimental basis for exploring more effective strategies for immune tolerance induced by sepsis.