血小板外泌体介导的PD-1/PD-L1通路在脓毒症中调控免疫细胞的作用机制
The Mechanism of Platelet Exosome-Mediated PD-1/PD-L1 Pathway in Regulating Immune Cells in Sepsis
DOI: 10.12677/acm.2025.1572091, PDF,    科研立项经费支持
作者: 李伟大, 胡爱民:吉首大学医学院,湖南 吉首;周建亮*:吉首大学第四临床医学院,湖南 怀化
关键词: 程序性死亡受体-1配体脓毒症单核细胞Programmed Death Receptor-1 Ligand Sepsis Monocyte
摘要: 脓毒症是由于感染导致宿主反应失调,从而引发的可能危及生命的器官功能障碍。从临床来看,无论是发病率还是病死率都是很高的。目前脓毒症的发病机制极其复杂,且发病机制仍不明确,目前未发现有效手段完全治愈,是重症监护病房(ICU)患者死亡的主要原因,这是当前危重症医学所研究的热门话题。同时,通过研究发现显示,免疫抑制是脓毒症最重要的病理生理改变,通过PD-1/PD-L1轴调控免疫细胞,从而进一步加剧免疫抑制程度。其中程序性死亡受体-1 (programmed death-1, PD-1)/程序性死亡受体-1配体(programmed death-1 ligand, PD-L1)分别为分化簇家族中的CD279和CD274,PD-1/PD-L1通路可通过调节T淋巴细胞活化及细胞耐受性在免疫调节中发挥关键作用。本文主要探讨脓毒症中血小板外泌体介导的PD-1/PD-L1对于各类免疫细胞的功能调控,从而为临床进一步提供证据。
Abstract: Sepsis is a potentially life-threatening organ dysfunction caused by the dysregulation of the host response due to infection. Clinically speaking, both the incidence rate and the fatality rate are very high. At present, the pathogenesis of sepsis is extremely complex and remains unclear. No effective means for a complete cure have been found so far. It is the main cause of death for patients in the intensive care unit (ICU), which is a hot topic currently studied in critical care medicine. Meanwhile, research findings show that immunosuppression is the most important pathophysiological change in sepsis. It regulates immune cells through the PD-1/PD-L1 axis, thereby further intensifying the degree of immunosuppression. Among them, programmed death-1 (PD-1)/programmed death-1 ligand (PD-L1) are CD279 and CD274 in the differentiation cluster family, respectively. The PD-1/PD-L1 pathway can play a key role in immune regulation by regulating the activation of T lymphocytes and cell tolerance. This article mainly explores the functional regulation of PD-1/PD-L1 mediated by platelet exosomes in septic blood on various immune cells, thereby providing further evidence for clinical practice.
文章引用:李伟大, 周建亮, 胡爱民. 血小板外泌体介导的PD-1/PD-L1通路在脓毒症中调控免疫细胞的作用机制[J]. 临床医学进展, 2025, 15(7): 1053-1058. https://doi.org/10.12677/acm.2025.1572091

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