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髓磷脂蛋白零肽诱导C57BL/6小鼠实验性自身免疫性神经炎。

Myelin Protein Zero Peptide Induced Experimental Autoimmune Neuritis in C57BL/6 Mice.

作者信息

Gonsalvez David G, Yoo SangWon, Craig Georgina A, Wood Rhiannon J, Fletcher Jessica L, Murray Simon S, Xiao Junhua

机构信息

Faculty of Medicine, Dentistry and Health Sciences, Department of Anatomy and Neuroscience, School of Biomedical Sciences, The University of Melbourne, Melbourne, VIC, Australia.

出版信息

Methods Mol Biol. 2018;1791:243-250. doi: 10.1007/978-1-4939-7862-5_19.

DOI:10.1007/978-1-4939-7862-5_19
PMID:30006715
Abstract

Mouse models of peripheral demyelinating neuropathy play an important role in enabling the study of disease pathogenesis. Further, induction in transgenic mice allows for the precise interrogation of disease mechanisms, as well as the analysis of the efficacy and mechanisms of potential new therapies. Here we describe a method to successfully induce experimental autoimmune neuritis (EAN) using myelin protein zero (P0) peptide in combination with Freund's complete adjuvant and pertussis toxin in the C57BL/6 mouse strain. We also outline a sensitive paradigm of accurately assessing the extent of functional deficits occurring in murine EAN.

摘要

外周脱髓鞘性神经病的小鼠模型在疾病发病机制的研究中发挥着重要作用。此外,在转基因小鼠中诱导发病能够精确探究疾病机制,还能分析潜在新疗法的疗效及作用机制。在此,我们描述一种在C57BL/6小鼠品系中使用髓鞘蛋白零(P0)肽联合弗氏完全佐剂和百日咳毒素成功诱导实验性自身免疫性神经炎(EAN)的方法。我们还概述了一种准确评估小鼠EAN中功能缺陷程度的灵敏方案。

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Myelin Protein Zero Peptide Induced Experimental Autoimmune Neuritis in C57BL/6 Mice.髓磷脂蛋白零肽诱导C57BL/6小鼠实验性自身免疫性神经炎。
Methods Mol Biol. 2018;1791:243-250. doi: 10.1007/978-1-4939-7862-5_19.
2
P0 protein peptide 180-199 together with pertussis toxin induces experimental autoimmune neuritis in resistant C57BL/6 mice.
J Neurosci Res. 2000 Dec 1;62(5):717-21. doi: 10.1002/1097-4547(20001201)62:5<717::AID-JNR11>3.0.CO;2-P.
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P0(106-125) is a neuritogenic epitope of the peripheral myelin protein P0 and induces autoimmune neuritis in C57BL/6 mice.
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Neutralizing antibodies to IL-18 ameliorate experimental autoimmune neuritis by counter-regulation of autoreactive Th1 responses to peripheral myelin antigen.抗白细胞介素-18中和抗体通过对自身反应性Th1细胞对外周髓鞘抗原反应的反向调节来改善实验性自身免疫性神经炎。
J Neuropathol Exp Neurol. 2002 Jul;61(7):614-22. doi: 10.1093/jnen/61.7.614.
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A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments.一种在C57BL/6小鼠中诱导实验性自身免疫性神经炎以进行功能和神经病理学评估的简单方法。
J Vis Exp. 2017 Nov 9(129):56455. doi: 10.3791/56455.
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The critical role of IL-12p40 in initiating, enhancing, and perpetuating pathogenic events in murine experimental autoimmune neuritis.IL-12p40在小鼠实验性自身免疫性神经炎的致病事件启动、增强和持续过程中的关键作用。
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Suppression of autoimmune neuritis in IFN-gamma receptor-deficient mice.干扰素-γ受体缺陷小鼠自身免疫性神经炎的抑制
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Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) blockade enhances incidence and severity of experimental autoimmune neuritis in resistant mice.细胞毒性T淋巴细胞相关抗原4(CTLA-4)阻断增强了抗性小鼠实验性自身免疫性神经炎的发病率和严重程度。
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CD28-B7 costimulation: a critical role for initiation and development of experimental autoimmune neuritis in C57BL/6 mice.CD28-B7共刺激:在C57BL/6小鼠实验性自身免疫性神经炎的起始和发展中起关键作用。
J Neuroimmunol. 2001 Mar 1;114(1-2):114-21. doi: 10.1016/s0165-5728(01)00241-7.
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CCR5 deficiency does not prevent P0 peptide 180-199 immunized mice from experimental autoimmune neuritis.CCR5缺陷并不能阻止经P0肽180 - 199免疫的小鼠发生实验性自身免疫性神经炎。
Neurobiol Dis. 2004 Aug;16(3):630-7. doi: 10.1016/j.nbd.2004.04.007.

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