Study progress of role of co-suppressor molecules in sepsis immune dysfunction
10.3760/cma.j.cn121430-20190916-00023
- VernacularTitle:共抑制分子在脓毒症免疫功能障碍中作用的研究进展
- Author:
Jinghua GAO
1
;
Zheying LIU
;
Zhifeng LIU
Author Information
1. 南方医科大学第一临床医学院，广州 510515；南部战区总医院重症医学科，广州 510010
- From:
Chinese Critical Care Medicine
2020;32(1):121-125
- CountryChina
- Language:Chinese
-
Abstract:
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. The pathophysiology core issue is that the body initiates a severe inflammatory reaction in response to the invasion of pathogenic microorganisms at the initial stage of disease. Subsequently, the body begins to fight inflammation in order to balance immunity status and eventually induces the immune paralysis or immunosuppressive state characterized by exhaustion of immune cell. Both in innate immunity and in acquired immunity, some co-suppressor molecules on the surface of immune cells play important roles in immunosuppression, such as, programmed death receptor-1 (PD-1), T cell immunoglobulin and mucin-containing protein-3 (TIM-3), cytotoxic T lymphocyte associated antigen-4 (CTLA-4), natural killer cell receptor 2B4 (CD244), B and T lymphocyte attenuator (BTLA) and NKG2A (CD94), et al. Blocking the interaction between these co-suppressor molecules and their ligands can significantly reverse the immunosuppressive state in septic animal models or patients. In order to provide a reference for the monitoring and treatment of sepsis immune dysfunction, this article mainly summarizes the new findings on the role of those co-suppressor molecules in sepsis immune dysfunction in recent years.
