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Animal models of Multiple Sclerosis.多发性硬化症的动物模型。
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2
Two models of multiple sclerosis: experimental allergic encephalomyelitis (EAE) and Theiler's murine encephalomyelitis virus (TMEV) infection. A pathological and immunological comparison.多发性硬化的两种模型：实验性变应性脑脊髓炎（EAE）和泰勒鼠脑脊髓炎病毒（TMEV）感染。病理与免疫学比较。
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3
Contrasting roles for axonal degeneration in an autoimmune versus viral model of multiple sclerosis: When can axonal injury be beneficial?轴突变性在自身免疫性与病毒性多发性硬化模型中的不同作用：轴突损伤何时有益？
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Mouse models of multiple sclerosis: experimental autoimmune encephalomyelitis and Theiler's virus-induced demyelinating disease.多发性硬化症的小鼠模型：实验性自身免疫性脑脊髓炎和泰勒氏病毒诱导的脱髓鞘疾病。
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Two models for multiple sclerosis: experimental allergic encephalomyelitis and Theiler's murine encephalomyelitis virus.多发性硬化症的两种模型：实验性变应性脑脊髓炎和泰勒氏鼠脑脊髓炎病毒。
J Neuropathol Exp Neurol. 1996 Jun;55(6):673-86. doi: 10.1097/00005072-199606000-00001.
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Neuropathogenesis of Theiler's murine encephalomyelitis virus infection, an animal model for multiple sclerosis.Theiler 氏鼠脑脊髓炎病毒感染的神经病理学，多发性硬化的动物模型。
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Periventricular demyelination and axonal pathology is associated with subependymal virus spread in a murine model for multiple sclerosis.脑室周围脱髓鞘和轴突病理学与多发性硬化症的鼠模型中的室管膜下病毒传播有关。
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Animal models of multiple sclerosis: Focus on experimental autoimmune encephalomyelitis.多发性硬化症的动物模型：聚焦实验性自身免疫性脑脊髓炎。
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Dihydroartemisinin enhances remyelination by switching microglia to the reparative phenotype.双氢青蒿素通过将小胶质细胞转变为修复性表型来增强髓鞘再生。
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MOG-induced EAE model of optic nerve inflammation compared to MS, MOGAD and NMOSD related subtypes of human optic neuritis.与多发性硬化症、MOG抗体相关疾病（MOGAD）和视神经脊髓炎谱系障碍（NMOSD）相关的人类视神经炎亚型相比，MOG诱导的视神经炎症性自身免疫性脑脊髓炎（EAE）模型。
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本文引用的文献

1
Regulatory T cells in autoimmune neuroinflammation.自身免疫性神经炎症中的调节性T细胞。
Immunol Rev. 2014 May;259(1):231-44. doi: 10.1111/imr.12169.
2
The selective anti-IL17A monoclonal antibody secukinumab (AIN457) attenuates IL17A-induced levels of IL6 in human astrocytes.选择性抗白细胞介素 17A 单克隆抗体司库珠单抗（AIN457）可减弱白细胞介素 17A 诱导的人星形胶质细胞中白细胞介素 6 的水平。
Glia. 2014 May;62(5):725-35. doi: 10.1002/glia.22637.
3
Protective and detrimental roles for regulatory T cells in a viral model for multiple sclerosis.调节性T细胞在多发性硬化症病毒模型中的保护和有害作用。
Brain Pathol. 2014 Sep;24(5):436-51. doi: 10.1111/bpa.12119. Epub 2014 Feb 25.
4
Cuprizone [bis(cyclohexylidenehydrazide)] is selectively toxic for mature oligodendrocytes.铜灰宁（环己叉二酰肼）对成熟的少突胶质细胞具有选择性毒性。
Neurotox Res. 2013 Aug;24(2):244-50. doi: 10.1007/s12640-013-9380-9. Epub 2013 Feb 8.
5
Bat3 promotes T cell responses and autoimmunity by repressing Tim-3–mediated cell death and exhaustion.Bat3 通过抑制 Tim-3 介导的细胞死亡和衰竭来促进 T 细胞反应和自身免疫。
Nat Med. 2012 Sep;18(9):1394-400. doi: 10.1038/nm.2871.
6
A transgenic model of central nervous system autoimmunity mediated by CD4+ and CD8+ T and B cells.由 CD4+ 和 CD8+ T 及 B 细胞介导的中枢神经系统自身免疫的转基因模型。
J Immunol. 2012 Mar 1;188(5):2084-92. doi: 10.4049/jimmunol.1102186. Epub 2012 Jan 25.
7
Experimental autoimmune encephalomyelitis--achievements and prospective advances.实验性自身免疫性脑脊髓炎——成就与展望。
APMIS. 2011 Dec;119(12):819-30. doi: 10.1111/j.1600-0463.2011.02794.x. Epub 2011 Oct 18.
8
The many faces of Th17 cells.Th17 细胞的多面性。
Curr Opin Immunol. 2011 Dec;23(6):702-6. doi: 10.1016/j.coi.2011.08.007. Epub 2011 Sep 6.
9
Identification of T helper type 1-like, Foxp3+ regulatory T cells in human autoimmune disease.在人类自身免疫性疾病中鉴定辅助性 T 细胞 1 样、Foxp3+调节性 T 细胞。
Nat Med. 2011 Jun;17(6):673-5. doi: 10.1038/nm.2389. Epub 2011 May 3.
10
Experimental models of multiple sclerosis.多发性硬化症的实验模型。
Curr Opin Neurol. 2011 Jun;24(3):291-9. doi: 10.1097/WCO.0b013e328346c226.

多发性硬化症的动物模型。

Animal models of Multiple Sclerosis.

作者信息

Procaccini Claudio, De Rosa Veronica, Pucino Valentina, Formisano Luigi, Matarese Giuseppe

机构信息

Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR) c/o Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università di Napoli "Federico II", 80131 Napoli, Italy.

Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR) c/o Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università di Napoli "Federico II", 80131 Napoli, Italy; Unità di NeuroImmunologia, IRCCS Fondazione Santa Lucia, 00143 Roma, Italy.

出版信息

Eur J Pharmacol. 2015 Jul 15;759:182-91. doi: 10.1016/j.ejphar.2015.03.042. Epub 2015 Mar 27.

DOI:10.1016/j.ejphar.2015.03.042
PMID:25823807
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7094661/
Abstract

Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) which involves a complex interaction between immune system and neural cells. Animal modeling has been critical for addressing MS pathogenesis. The three most characterized animal models of MS are (1) the experimental autoimmune/allergic encephalomyelitis (EAE); (2) the virally-induced chronic demyelinating disease, known as Theiler׳s murine encephalomyelitis virus (TMEV) infection and (3) the toxin-induced demyelination. All these models, in a complementary way, have allowed to reach a good knowledge of the pathogenesis of MS. Specifically, EAE is the model which better reflects the autoimmune pathogenesis of MS and is extremely useful to study potential experimental treatments. Furthermore, both TMEV and toxin-induced demyelination models are suitable for characterizing the role of the axonal injury/repair and the remyelination process in MS. In conclusion, animal models, despite their limitations, remain the most useful instrument for implementing the study of MS.

摘要

多发性硬化症（MS）是一种中枢神经系统（CNS）的炎性脱髓鞘疾病，涉及免疫系统和神经细胞之间的复杂相互作用。动物模型对于阐明MS的发病机制至关重要。MS的三种最具特征性的动物模型是：（1）实验性自身免疫性/过敏性脑脊髓炎（EAE）；（2）病毒诱导的慢性脱髓鞘疾病，即泰勒氏鼠脑脊髓炎病毒（TMEV）感染；以及（3）毒素诱导的脱髓鞘。所有这些模型以互补的方式，使人们对MS的发病机制有了很好的了解。具体而言，EAE是最能反映MS自身免疫发病机制的模型，对研究潜在的实验性治疗方法极为有用。此外，TMEV和毒素诱导的脱髓鞘模型都适用于表征轴突损伤/修复和MS中髓鞘再生过程的作用。总之，动物模型尽管有其局限性，但仍然是开展MS研究最有用的工具。