Dendritic cells as master regulators of the T-cell axis in sepsis: mechanisms and therapeutic implications

Sepsis is a life-threatening systemic inflammatory response syndrome triggered by infection, characterized by profound dysregulation of the immune system. Dendritic cells (DCs), which serve as the essential bridge between innate and adaptive immunity, play a critical role in the pathogenesis and progression of sepsis. The functional status of DCs profoundly influences the activation, differentiation, and function of T cells, thereby determining disease outcomes. This review systematically summarizes the dynamic changes in the developmental lineage and functional phenotype of DCs in the context of sepsis, as well as their multi-layered regulatory mechanisms governing T cell responses. We focus on the molecular basis of sepsis-induced DC dysfunction—including apoptosis, exhaustion, and immunoparalysis—and the resulting T cell immunosuppression. Finally, we discuss current progress in intervention strategies aimed at restoring T cell immune homeostasis by modulating DC function, providing a theoretical foundation for understanding the immunopathology of sepsis and developing novel immunotherapies.