Gold R, Hartung H P, Toyka K V
Department of Neurology, University of Wurzburg, Neurologische Universitätsklinik, Josef-Schneider-Str. 11, 97080 Würzburg, Germany.
Mol Med Today. 2000 Feb;6(2):88-91. doi: 10.1016/s1357-4310(99)01639-1.
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) that takes a relapsing-remitting or a progressive course (reviewed in Refs 1,2). Its counterpart in the peripheral nervous system (PNS) is chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) (reviewed in Ref. 3). In addition, there are acute, monophasic disorders, such as the inflammatory demyelinating polyradiculoneuropathy termed Guillain-Barré syndrome (GBS) in the PNS, and acute disseminated encephalomyelitis (ADEM) in the CNS. Both MS and GBS are heterogeneous syndromes. In MS different exogenous assaults together with genetic factors can result in a disease course that finally fulfils the diagnostic criteria. In both diseases, axonal damage can add to a primarily demyelinating lesion and cause permanent neurological deficits. No single animal model exists that mimics all the features of human demyelinating diseases; rather, the available models reflect specific facets. Here, we focus on experimental autoimmune encephalomyelitis (EAE) and neuritis (EAN) as models in rat and mouse strains, and discuss their distinct histopathology and the roles played by different autoantigens.
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，呈复发-缓解型或进行性病程（参考文献1,2中有综述）。其在外周神经系统（PNS）中的对应疾病是慢性炎性脱髓鞘性多发性神经根神经病（CIDP）（参考文献3中有综述）。此外，还有急性单相性疾病，如PNS中称为吉兰-巴雷综合征（GBS）的炎性脱髓鞘性多发性神经根神经病，以及CNS中的急性播散性脑脊髓炎（ADEM）。MS和GBS都是异质性综合征。在MS中，不同的外源性攻击与遗传因素共同作用可导致最终符合诊断标准的病程。在这两种疾病中，轴突损伤可加重原发性脱髓鞘病变并导致永久性神经功能缺损。不存在能模拟人类脱髓鞘疾病所有特征的单一动物模型；相反，现有的模型反映了特定的方面。在此，我们重点关注大鼠和小鼠品系中的实验性自身免疫性脑脊髓炎（EAE）和神经炎（EAN）模型，并讨论它们独特的组织病理学以及不同自身抗原所起的作用。
