摘要脓毒症定义为由宿主对感染的反应失调引起的危及生命的器官功能障碍。脓毒症发生时，T淋巴细胞（T细胞）不仅通过特异性杀伤作用清除靶细胞，还响应抗原呈递信号并辅助B淋巴细胞介导体液免疫，因此T细胞分化亚群数量和功能的维持十分重要。脓毒症打破了宿主效应T细胞亚群的稳定状态，导致淋巴细胞数量减少和功能缺失，并在细胞丢失和获得的多个方面影响T细胞池稳定，进而触发持久的免疫抑制状态。据报道，多种细胞死亡和增殖调节机制参与了该稳态的失衡修复过程。本文就效应T细胞亚群数量与质量稳态的发展变化及其参与脓毒症免疫抑制的可能机制进行综述。

abstractsSepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. The maintenance of T lymphocyte subpopulation abundance and function is of great significance during sepsis, as T lymphocytes not only eliminate target cells by specific killing effect but also respond to antigen-presentation signals and assist B lymphocyte-mediated humoral immunity. Sepsis disrupts the homeostasis of effector T lymphocyte subsets, leading to lymphocytopenia, functional deficits, and affecting the stability of the T lymphocyte pool in many aspects of cell loss and acquisition, which in turn triggers persistent immunosuppression. Multiple mechanisms of cell death and proliferation have been reported to be involved in the dyshomeostasis and repair of T lymphocyte homeostasis. The article reviews the development of quantity and quality over homeostasis in effector T lymphocyte subsets and the possible mechanisms involved in immunosuppression in sepsis.