Dendritic cells as master regulators of the T-cell axis in sepsis: mechanisms and therapeutic implications
7 affiliations
- 1Department of Anesthesiology, The First People’s Hospital of Chenzhou, The First Clinical College, Xiangnan University
- 2Department of Intensive Care Unit, The First Affiliated Hospital of Jinan University
- 3Department of Critical Care Medicine, The First People’s Hospital of Chenzhou, The First School of Clinical Medicine, Southern Medical University
- 4Department of Pathology, The First People's Hospital of Chenzhou, The First Clinical College, Xiangnan University
- 5Department of Anesthesiology, Guiyang County Maternal and Child Health Hospital
- 6Department of Gastroenterology, The First People’s Hospital of Chenzhou, The First Clinical College, Xiangnan University
- 7Department of Anesthesiology, Toksun County People's Hospital
Abstract
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.
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BibTeX
@article{li2026dendritic,
title = {{Dendritic cells as master regulators of the T-cell axis in sepsis: mechanisms and therapeutic implications}},
author = {Zhiwang Li and Xiang-Jie Duan and Tao Li and Xiaoyong Gong and Jinru Li and Bo Li and Jiayi He and Fangqing Luo and Fangfang Li and Peiyu Li and Zhiming Zhang},
journal = {Frontiers in Immunology},
year = {2026},
month = nov,
doi = {10.3389/fimmu.2026.1961624},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1961624/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Dendritic cells as master regulators of the T-cell axis in sepsis: mechanisms and therapeutic implications
AU - Zhiwang Li
AU - Xiang-Jie Duan
AU - Tao Li
AU - Xiaoyong Gong
AU - Jinru Li
AU - Bo Li
AU - Jiayi He
AU - Fangqing Luo
AU - Fangfang Li
AU - Peiyu Li
AU - Zhiming Zhang
PY - 2026
DA - 2026/11/02
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1961624
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1961624/full
AB - 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.
SN - 1664-3224
ER -