Animal models for autoimmune demyelinating disorders of the nervous system

Animal models for autoimmune demyelinating disorders of the nervous system
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DOI:
10.1016/s1357-4310(99)01639-1
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发表时间:
2000-02-01
期刊:
MOLECULAR MEDICINE TODAY
影响因子:
--
通讯作者:
Toyka, KV
Toyka, KV
中科院分区:
其他
文献类型:
--
作者:
Gold, R;Hartung, HP;Toyka, KV

文献摘要

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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,具有复发-缓解或进行性病程(综述见参考文献1、2)。其在周围神经系统(PNS)中的对应物是慢性炎性脱髓鞘性多发性神经根神经病(CIDP)(综述见参考文献3)。此外,还存在急性、多相性疾病,如PNS中称为格林-巴利综合征(GBS)的炎性脱髓鞘性多神经根神经病和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一起可导致最终满足诊断标准的疾病过程。在这两种疾病中,轴突损伤可以增加主要的脱髓鞘病变,并导致永久性神经功能缺损。没有一种动物模型能够模仿人类脱髓鞘疾病的所有特征;相反,现有的模型反映了特定的方面。在这里,我们专注于实验性自身免疫性脑脊髓炎(EAE)和神经炎(EAN)作为模型在大鼠和小鼠品系,并讨论其不同的组织病理学和不同的自身抗原所发挥的作用。
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.