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本文引用的文献

1
Targeting the programmed cell death 1: programmed cell death ligand 1 pathway reverses T cell exhaustion in patients with sepsis.靶向程序性细胞死亡蛋白1:程序性细胞死亡配体1通路可逆转脓毒症患者的T细胞耗竭。
Crit Care. 2014 Jan 4;18(1):R3. doi: 10.1186/cc13176.
2
BTLA as a biomarker and mediator of sepsis-induced immunosuppression.BTLA作为脓毒症诱导免疫抑制的生物标志物和介质。
Crit Care. 2013 Dec 9;17(6):1022. doi: 10.1186/cc13143.
3
Negative role of inducible PD-1 on survival of activated dendritic cells.诱导型 PD-1 对激活的树突状细胞存活的负向作用。
J Leukoc Biol. 2014 Apr;95(4):621-9. doi: 10.1189/jlb.0813443. Epub 2013 Dec 6.
4
B and T lymphocyte attenuator expression on CD4+ T-cells associates with sepsis and subsequent infections in ICU patients.CD4+ T细胞上B和T淋巴细胞衰减器的表达与ICU患者的败血症及随后的感染相关。
Crit Care. 2013 Nov 29;17(6):R276. doi: 10.1186/cc13131.
5
Histones-mediated lymphocyte apoptosis during sepsis is dependent on p38 phosphorylation and mitochondrial permeability transition.脓毒症中组蛋白介导的淋巴细胞凋亡依赖于 p38 磷酸化和线粒体通透性转换。
PLoS One. 2013 Oct 22;8(10):e77131. doi: 10.1371/journal.pone.0077131. eCollection 2013.
6
The significance and regulatory mechanisms of innate immune cells in the development of sepsis.固有免疫细胞在脓毒症发生发展中的意义及其调控机制。
J Interferon Cytokine Res. 2014 Jan;34(1):2-15. doi: 10.1089/jir.2013.0042. Epub 2013 Sep 5.
7
Enhancing specific-antibody production to the ragB vaccine with GITRL that expand Tfh, IFN-γ(+) T cells and attenuates Porphyromonas gingivalis infection in mice.用 GITRL 增强 RagB 疫苗的特异性抗体产生,从而扩增 Tfh、IFN-γ(+) T 细胞,并减轻小鼠牙龈卟啉单胞菌感染。
PLoS One. 2013;8(4):e59604. doi: 10.1371/journal.pone.0059604. Epub 2013 Apr 1.
8
Dendritic cell apoptosis and the pathogenesis of dengue.树突状细胞凋亡与登革热发病机制。
Viruses. 2012 Nov 1;4(11):2736-53. doi: 10.3390/v4112736.
9
Renal cell apoptosis and new treatment options in sepsis-induced acute kidney injury.脓毒症诱导的急性肾损伤中的肾细胞凋亡和新的治疗选择。
Ren Fail. 2013;35(2):291-4. doi: 10.3109/0886022X.2012.744040. Epub 2012 Nov 27.
10
Monocytes regulate the mechanism of T-cell death by inducing Fas-mediated apoptosis during bacterial infection.单核细胞在细菌感染过程中通过诱导 Fas 介导线粒体凋亡来调节 T 细胞死亡的机制。
PLoS Pathog. 2012;8(7):e1002814. doi: 10.1371/journal.ppat.1002814. Epub 2012 Jul 19.

脓毒症中免疫细胞凋亡性死亡的相关见解。

Insights into the apoptotic death of immune cells in sepsis.

作者信息

Luan Ying-yi, Yao Yong-ming, Xiao Xian-zhong, Sheng Zhi-yong

机构信息

1 Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital , Beijing, People's Republic of China .

出版信息

J Interferon Cytokine Res. 2015 Jan;35(1):17-22. doi: 10.1089/jir.2014.0069. Epub 2014 Jul 9.

DOI:10.1089/jir.2014.0069
PMID:25007137
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4291200/
Abstract

Sepsis with subsequent multiple-organ dysfunction is a distinct systemic inflammatory response to concealed or obvious infection, and it is a leading cause of death in intensive care units. Thus, one of the key goals in critical care medicine is to develop novel therapeutic strategies that will affect favorably on outcome of septic patients. In addition to systemic response to infection, apoptosis is implicated to be an important mechanism of the death of immune cells, including neutrophils, macrophages, T lymphocytes, and dendritic cells, and it is usually followed by the development of multiple-organ failure in sepsis. The implication of apoptosis of immune cells is now highlighted by multiple studies that demonstrate that prevention of cell apoptosis can improve survival in relevant animal models of severe sepsis. In this review, we focus on major apoptotic death pathways and molecular mechanisms that regulate apoptosis of different immune cells, and advances in these areas that may be translated into more promising therapies for the prevention and treatment of severe sepsis.

摘要

伴有随后多器官功能障碍的脓毒症是对隐匿性或显性感染的一种独特的全身炎症反应,并且是重症监护病房中死亡的主要原因。因此,重症医学的关键目标之一是开发能对脓毒症患者的预后产生有利影响的新型治疗策略。除了对感染的全身反应外,细胞凋亡被认为是免疫细胞死亡的重要机制,包括中性粒细胞、巨噬细胞、T淋巴细胞和树突状细胞,并且在脓毒症中通常随后会发生多器官衰竭。多项研究突出了免疫细胞凋亡的影响,这些研究表明预防细胞凋亡可提高严重脓毒症相关动物模型的存活率。在本综述中,我们聚焦于调节不同免疫细胞凋亡的主要凋亡死亡途径和分子机制,以及这些领域的进展,这些进展可能转化为预防和治疗严重脓毒症更有前景的疗法。