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本文引用的文献

1
Gut microbiota lipopolysaccharide accelerates inflamm-aging in mice.肠道微生物群脂多糖加速小鼠炎症衰老。
BMC Microbiol. 2016 Jan 16;16:9. doi: 10.1186/s12866-016-0625-7.
2
Inflammation, But Not Telomere Length, Predicts Successful Ageing at Extreme Old Age: A Longitudinal Study of Semi-supercentenarians.炎症而非端粒长度可预测高龄老人的成功衰老:对半超级百岁老人的纵向研究
EBioMedicine. 2015 Jul 29;2(10):1549-58. doi: 10.1016/j.ebiom.2015.07.029. eCollection 2015 Oct.
3
Monocyte and macrophage subsets along the continuum to heart failure: Misguided heroes or targetable villains?单核细胞和巨噬细胞亚群在心力衰竭连续过程中的作用:是误入歧途的英雄还是可靶向的反派?
J Mol Cell Cardiol. 2015 Dec;89(Pt B):136-45. doi: 10.1016/j.yjmcc.2015.10.029. Epub 2015 Oct 28.
4
Cardiorespiratory Fitness in Middle Age and Health Care Costs in Later Life.中年时期的心肺适能与晚年的医疗保健费用。
J Am Coll Cardiol. 2015 Oct 27;66(17):1876-85. doi: 10.1016/j.jacc.2015.08.030.
5
Differential Gene Expression Profiles Reflecting Macrophage Polarization in Aging and Periodontitis Gingival Tissues.反映衰老和牙周炎牙龈组织中巨噬细胞极化的差异基因表达谱
Immunol Invest. 2015;44(7):643-64. doi: 10.3109/08820139.2015.1070269. Epub 2015 Sep 23.
6
Current Concept and Update of the Macrophage Plasticity Concept: Intracellular Mechanisms of Reprogramming and M3 Macrophage "Switch" Phenotype.巨噬细胞可塑性概念的当前认识与更新:重编程的细胞内机制及M3巨噬细胞“转换”表型
Biomed Res Int. 2015;2015:341308. doi: 10.1155/2015/341308. Epub 2015 Aug 23.
7
Age decreases macrophage IL-10 expression: Implications for functional recovery and tissue repair in spinal cord injury.年龄降低巨噬细胞白细胞介素-10的表达:对脊髓损伤后功能恢复和组织修复的影响。
Exp Neurol. 2015 Nov;273:83-91. doi: 10.1016/j.expneurol.2015.08.001. Epub 2015 Aug 8.
8
CD73 Activity is Dispensable for the Polarization of M2 Macrophages.CD73活性对于M2巨噬细胞的极化并非必需。
PLoS One. 2015 Aug 10;10(8):e0134721. doi: 10.1371/journal.pone.0134721. eCollection 2015.
9
E-cadherin expression in macrophages dampens their inflammatory responsiveness in vitro, but does not modulate M2-regulated pathologies in vivo.巨噬细胞中E-钙黏蛋白的表达在体外会减弱其炎症反应,但在体内不会调节M2相关的病理过程。
Sci Rep. 2015 Jul 31;5:12599. doi: 10.1038/srep12599.
10
Intestinal CD169(+) macrophages initiate mucosal inflammation by secreting CCL8 that recruits inflammatory monocytes.肠道CD169(+)巨噬细胞通过分泌招募炎性单核细胞的CCL8引发黏膜炎症。
Nat Commun. 2015 Jul 21;6:7802. doi: 10.1038/ncomms8802.

高龄会改变单核细胞和巨噬细胞的反应。

Advanced Age Alters Monocyte and Macrophage Responses.

作者信息

Albright Joslyn M, Dunn Robert C, Shults Jill A, Boe Devin M, Afshar Majid, Kovacs Elizabeth J

机构信息

1 Department of Surgery, Loyola University Chicago Health Sciences Campus , Maywood, Illinois.

2 Burn and Shock Trauma Research Institute, Loyola University Chicago Health Sciences Campus , Maywood, Illinois.

出版信息

Antioxid Redox Signal. 2016 Nov 20;25(15):805-815. doi: 10.1089/ars.2016.6691. Epub 2016 Aug 3.

DOI:10.1089/ars.2016.6691
PMID:27357201
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5107740/
Abstract

SIGNIFICANCE

With the growing population of baby boomers, there is a great need to determine the effects of advanced age on the function of the immune system. Recent Advances: It is universally accepted that advanced age is associated with a chronic low-grade inflammatory state that is referred to as inflamm-aging, which alters the function of both immune and nonimmune cells. Mononuclear phagocytes play a central role in both the initiation and resolution of inflammation in multiple organ systems and exhibit marked changes in phenotype and function in response to environmental cues, including the low levels of pro-inflammatory mediators seen in the aged.

CRITICAL ISSUES

Although we know a great deal about the function of immune cells in young adults and there is a growing body of literature focusing on aging of the adaptive immune system, much less is known about the impact of age on innate immunity and the critical role of the mononuclear phagocytes in this process.

FUTURE DIRECTIONS

In this article, there is a focus on the tissue-specific monocyte and macrophage subsets and how they are altered in the aged milieu, with the hope that this compilation of observations will spark an expansion of research in the field. Antioxid. Redox Signal. 25, 805-815.

摘要

意义

随着婴儿潮一代人口的不断增加,迫切需要确定高龄对免疫系统功能的影响。最新进展:人们普遍认为,高龄与一种被称为炎症衰老的慢性低度炎症状态相关,这种状态会改变免疫细胞和非免疫细胞的功能。单核吞噬细胞在多个器官系统炎症的起始和消退过程中都起着核心作用,并且会根据环境信号(包括老年人中所见的低水平促炎介质)在表型和功能上表现出显著变化。

关键问题

尽管我们对年轻成年人免疫细胞的功能了解很多,并且关注适应性免疫系统衰老的文献也越来越多,但对于年龄对固有免疫的影响以及单核吞噬细胞在此过程中的关键作用却知之甚少。

未来方向

在本文中,重点关注组织特异性单核细胞和巨噬细胞亚群以及它们在老年环境中的变化,希望这些观察结果的汇总能够激发该领域研究的扩展。《抗氧化. 氧化还原信号》25, 805 - 815。