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适应性免疫调节与脑缺血。

Adaptive Immunity Regulation and Cerebral Ischemia.

机构信息

Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.

Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, United States.

出版信息

Front Immunol. 2020 May 12;11:689. doi: 10.3389/fimmu.2020.00689. eCollection 2020.

DOI:10.3389/fimmu.2020.00689
PMID:32477327
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7235404/
Abstract

Stroke is a disease that occurs due to a sudden interruption of the blood supply to the brain. It is a leading cause of death and disability worldwide. It is well-known that the immune system drives brain injury following an episode of ischemic stroke. The innate system and the adaptive system play distinct but synergistic roles following ischemia. The innate system can be activated by damage-associated molecular patterns (DAMPs), which are released from cells in the ischemic region. Damaged cells also release various other mediators that serve to increase inflammation and compromise the integrity of the blood-brain barrier (BBB). Within 24 h of an ischemic insult, the adaptive immune system is activated. This involves T cell and B cell-mediated inflammatory and humoral effects. These cells also stimulate the release of various interleukins and cytokines, which can modulate the inflammatory response. The adaptive immune system has been shown to contribute to a state of immunodepression following an ischemic episode, and this can increase the risk of infections. However, this phenomenon is equally important in preventing autoimmunity of the body to brain antigens that are released into the peripheral system as a result of BBB compromise. In this review, we highlight the key components of the adaptive immune system that are activated following cerebral ischemia.

摘要

中风是一种由于大脑供血突然中断而引起的疾病。它是全球范围内导致死亡和残疾的主要原因。众所周知,免疫系统会在缺血性中风发作后引发脑损伤。固有免疫系统和适应性免疫系统在缺血后发挥着不同但协同的作用。固有免疫系统可以被损伤相关分子模式(DAMPs)激活,这些 DAMPs 是从缺血区域的细胞中释放出来的。受损细胞还会释放各种其他介质,这些介质会增加炎症并损害血脑屏障(BBB)的完整性。在缺血性损伤后的 24 小时内,适应性免疫系统被激活。这涉及 T 细胞和 B 细胞介导的炎症和体液效应。这些细胞还会刺激各种白细胞介素和细胞因子的释放,从而调节炎症反应。适应性免疫系统已被证明会导致缺血性发作后免疫抑制状态增加感染风险。然而,这种现象在预防因 BBB 受损而释放到外周系统的脑抗原引起的自身免疫方面同样重要。在这篇综述中,我们强调了在脑缺血后被激活的适应性免疫系统的关键组成部分。

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Sex differences in T cell immune responses, gut permeability and outcome after ischemic stroke in aged mice.老年小鼠缺血性脑卒中后 T 细胞免疫反应、肠道通透性和结局的性别差异。
Brain Behav Immun. 2020 Jul;87:556-567. doi: 10.1016/j.bbi.2020.02.001. Epub 2020 Feb 11.
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FasL-PDPK1 Pathway Promotes the Cytotoxicity of CD8 T Cells During Ischemic Stroke.FasL-PDPK1 通路在缺血性脑卒中期间促进 CD8 T 细胞的细胞毒性。
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Depletion of CD4 T cells provides therapeutic benefits in aged mice after ischemic stroke.
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Prognostic Impact of Neutrophil-to-Lymphocyte Ratio in Ischemic Stroke.中性粒细胞与淋巴细胞比值对缺血性卒中的预后影响
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Calycosin Ameliorates Neuroinflammation via TLR4-Mediated Signal Following Cerebral Ischemia/Reperfusion Injury in vivo and in vitro.毛蕊异黄酮通过TLR4介导的信号通路改善体内外脑缺血/再灌注损伤后的神经炎症。
J Inflamm Res. 2024 Dec 10;17:10711-10727. doi: 10.2147/JIR.S480262. eCollection 2024.
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Transplantation of Lymphocytes Co-Cultured with Human Cord Blood-Derived Multipotent Stem Cells Attenuates Inflammasome Activity in Ischemic Stroke.人脐带来源多能干细胞共培养的淋巴细胞移植可减轻缺血性脑卒中的炎症小体活性。
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ACC1 (Acetyl Coenzyme A Carboxylase 1) Is a Potential Immune Modulatory Target of Cerebral Ischemic Stroke.乙酰辅酶 A 羧化酶 1 是脑缺血性脑卒中的潜在免疫调节靶点。
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