Decoding the potential role of regulatory T cells in sepsis-induced immunosuppression.
Siyuan HuangDi LiuLei HanJin DengZhen WangJianxin JiangLing ZengPublished in: European journal of immunology (2024)
Sepsis, a multiorgan dysfunction with high incidence and mortality, is caused by an imbalanced host-to-infection immune response. Organ-support therapy improves the early survival rate of sepsis patients. In the long term, those who survive the "cytokine storm" and its secondary damage usually show higher susceptibility to secondary infections and sepsis-induced immunosuppression, in which regulatory T cells (Tregs) are evidenced to play an essential role. However, the potential role and mechanism of Tregs in sepsis-induced immunosuppression remains elusive. In this review, we elucidate the role of different functional subpopulations of Tregs during sepsis and then review the mechanism of sepsis-induced immunosuppression from the aspects of regulatory characteristics, epigenetic modification, and immunometabolism of Tregs. Thoroughly understanding how Tregs impact the immune system during sepsis may shed light on preclinical research and help improve the translational value of sepsis immunotherapy.
Keyphrases
- septic shock
- regulatory t cells
- acute kidney injury
- intensive care unit
- immune response
- high glucose
- diabetic rats
- dendritic cells
- oxidative stress
- end stage renal disease
- gene expression
- risk factors
- cardiovascular disease
- dna methylation
- chronic kidney disease
- ejection fraction
- transcription factor
- bone marrow
- peritoneal dialysis