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中枢神经系统侵袭需要T细胞迁移能力。

T-cell trafficking competence is required for CNS invasion.

作者信息

Lees Jason R, Archambault Angela S, Russell John H

机构信息

Department of Molecular Biology and Pharmacology, Campus Box 8103, 660 South Euclid, Washington University, St. Louis 63110, USA.

出版信息

J Neuroimmunol. 2006 Aug;177(1-2):1-10. doi: 10.1016/j.jneuroim.2006.05.024. Epub 2006 Jul 5.

DOI:10.1016/j.jneuroim.2006.05.024
PMID:16822552
Abstract

T-cell invasion of the CNS is critical for the induction of a variety of autoimmune mediated neuronal diseases. We utilized blood-brain barrier (BBB) mediated exclusion of anti-CD4 antibody to define populations of encephalitogenic T-cells recovered from mouse CNS preparations as either CNS invasive or non-invasive. This separation of cells allowed flow cytometric examination of the kinetics of encephalitogenic T-cell entry past the BBB. Further experiments examined the relative contribution of EAE inflammatory conditioning of the BBB to the kinetics of T-cell adherence and migration into the CNS. Inflammatory conditioning was found to have no effect on accumulation of T-cells at the vascular interface of the BBB, but was found to increase the entry of adoptively transferred T-cells into the CNS following their initial adherence to the BBB.

摘要

T细胞侵入中枢神经系统对于引发多种自身免疫介导的神经元疾病至关重要。我们利用血脑屏障(BBB)介导的抗CD4抗体排除法,将从小鼠中枢神经系统制剂中回收的致脑炎性T细胞群体定义为中枢神经系统侵入性或非侵入性。这种细胞分离使得能够通过流式细胞术检测致脑炎性T细胞穿过血脑屏障进入的动力学。进一步的实验研究了血脑屏障的实验性自身免疫性脑脊髓炎(EAE)炎症预处理对T细胞黏附和迁移至中枢神经系统动力学的相对贡献。结果发现,炎症预处理对血脑屏障血管界面处T细胞的积聚没有影响,但在过继转移的T细胞最初黏附于血脑屏障后,发现其能增加这些T细胞进入中枢神经系统的量。

相似文献

1
T-cell trafficking competence is required for CNS invasion.中枢神经系统侵袭需要T细胞迁移能力。
J Neuroimmunol. 2006 Aug;177(1-2):1-10. doi: 10.1016/j.jneuroim.2006.05.024. Epub 2006 Jul 5.
2
Encephalitogenic T-cells increase numbers of CNS T-cells regardless of antigen specificity by both increasing T-cell entry and preventing egress.致炎 T 细胞通过增加 T 细胞进入和阻止 T 细胞迁出,无论抗原特异性如何,都会增加中枢神经系统 T 细胞的数量。
J Neuroimmunol. 2010 Mar 30;220(1-2):10-6. doi: 10.1016/j.jneuroim.2009.11.017. Epub 2010 Feb 18.
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Defining antigen-dependent stages of T cell migration from the blood to the central nervous system parenchyma.定义T细胞从血液迁移至中枢神经系统实质的抗原依赖性阶段。
Eur J Immunol. 2005 Apr;35(4):1076-85. doi: 10.1002/eji.200425864.
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Blockade of the kinin receptor B1 protects from autoimmune CNS disease by reducing leukocyte trafficking.阻断激肽受体 B1 可通过减少白细胞迁移来预防自身免疫性中枢神经系统疾病。
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5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside attenuates experimental autoimmune encephalomyelitis via modulation of endothelial-monocyte interaction.5-氨基咪唑-4-甲酰胺-1-β-D-呋喃核糖苷通过调节内皮细胞与单核细胞的相互作用减轻实验性自身免疫性脑脊髓炎。
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Lack of junctional adhesion molecule (JAM)-B ameliorates experimental autoimmune encephalomyelitis.缺乏连接黏附分子(JAM)-B 可改善实验性自身免疫性脑脊髓炎。
Brain Behav Immun. 2018 Oct;73:3-20. doi: 10.1016/j.bbi.2018.06.014. Epub 2018 Jun 18.
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CNS-irrelevant T-cells enter the brain, cause blood-brain barrier disruption but no glial pathology.与中枢神经系统无关的T细胞进入大脑,导致血脑屏障破坏,但无神经胶质病理改变。
Eur J Neurosci. 2007 Sep;26(6):1387-98. doi: 10.1111/j.1460-9568.2007.05792.x.
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Immune-related GTPase Irgm1 exacerbates experimental auto-immune encephalomyelitis by promoting the disruption of blood-brain barrier and blood-cerebrospinal fluid barrier.免疫相关 GTPase Irgm1 通过促进血脑屏障和血脑脊液屏障的破坏加剧实验性自身免疫性脑脊髓炎。
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Suppression of experimental autoimmune encephalomyelitis by selective blockade of encephalitogenic T-cell infiltration of the central nervous system.通过选择性阻断致脑炎性T细胞向中枢神经系统的浸润来抑制实验性自身免疫性脑脊髓炎
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CXCR3 blockade inhibits T-cell migration into the CNS during EAE and prevents development of adoptively transferred, but not actively induced, disease.CXCR3 阻断可抑制 EAE 期间 T 细胞向中枢神经系统迁移,并防止过继转移但不主动诱导的疾病的发展。
Eur J Immunol. 2010 Oct;40(10):2751-61. doi: 10.1002/eji.200939975.

引用本文的文献

1
Pre-existing central nervous system lesions negate cytokine requirements for regional experimental autoimmune encephalomyelitis development.预先存在的中枢神经系统病变否定了细胞因子在区域性实验性自身免疫性脑脊髓炎发展中的需求。
Immunology. 2013 Mar;138(3):208-15. doi: 10.1111/imm.12029.
2
IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-beta.转化生长因子-β对白细胞介素-17信号非依赖性中枢神经系统自身免疫起负性调节作用。
J Immunol. 2009 Mar 1;182(5):2665-71. doi: 10.4049/jimmunol.0802221.