Mechanism of TREX1-mediated immune regulation and its role in sepsis
10.3760/cma.j.cn121430-20231121-01001
- VernacularTitle:TREX1介导的免疫调控机制及其在脓毒症中的作用研究进展
- Author:
Jing XIE
1
;
Qilan LI
;
Chenggang GAO
;
Yajun HE
;
Jiqian XU
;
You SHANG
Author Information
1. 华中科技大学同济医学院附属协和医院重症医学科，湖北武汉 430022
- Keywords:
Sepsis;
Three prime repair exonuclease 1;
Immune regulation
- From:
Chinese Critical Care Medicine
2024;36(8):877-881
- CountryChina
- Language:Chinese
-
Abstract:
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Sepsis-induced cell lysis and necrosis lead to the passive release of mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) into circulation. These DNAs bind to pattern recognition receptor (PRR), triggering excessive inflammatory cytokines production and increasing mortality. Three prime repair exonuclease 1 (TREX1) is a 3' to 5' exonuclease that rapidly degrades single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) by cleaving phosphodiester bonds. This process can prevent the accumulation of damaged DNA in the cytoplasm, thereby averting abnormal inflammation and pathological immune responses. TREX1 thus plays a significant role in regulating DNA-related damage caused by sepsis. However, the role and underlying mechanisms of TREX1 in sepsis have not been thoroughly discussed. This review aims to elucidate the structure and function of TREX1 and its mediated immune regulatory mechanisms, with the hope of clarifying the potential role of TREX1 in the field of sepsis.
