Sepsis 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.