豚鼠慢性实验性变应性脑脊髓炎的一种新形式的脱髓鞘大基底下斑块。

E C Alvord, B F Driscoll, M W Kies
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引用次数: 14

摘要

本报告描述了一种在成年豚鼠13株中产生慢性实验性变应性脑脊髓炎(EAE)+伴脱髓鞘的新技术。该疾病是由对髓鞘碱性蛋白(BP)敏感的淋巴结细胞的被动转移和同源脊髓受体在Freund的完全佐剂中的主动攻击相结合引起的。临床-病理谱范围从导致4-7周死亡的渐进性致死性慢性EAE,到缓解-复发型,再到持续数月的慢性稳定型。在所有这些形式中,大的脱髓鞘下斑块发生在脊髓,髓鞘碎片被活跃地吞噬,尤其是在边缘。轴突肿胀,但始终保持完整。病变的组织学表现表明,髓磷脂的溶解发生在吞噬作用之前,这是多发性硬化症患者病变发病机制的假设之一。
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Large subpial plaques of demyelination in a new form of chronic experimental allergic encephalomyelitis in the guinea pig.

The current report describes a new technique for producing chronic experimental allergic encephalomyelitis (EAE)+ accompanied by demyelination in adult strain 13 guinea pigs. The disease is induced by a combination of passive transfer of lymph node cells sensitized to myelin basic protein (BP) and active challenge of the recipients with homologous spinal cord in Freund's complete adjuvants. The clinical-pathologic spectrum ranges from a progressively fatal form of chronic EAE leading to death in 4-7 wk, through a remitting-relapsing form, to a chronic-stable form lasting many months. In all of these forms large subpial plaques of demyelination occur in the spinal cord with active phagocytosis of myelin debris, especially at the edges. The axons are swollen, but remain intact throughout. The histologic appearances of the lesions suggest that lysis of myelin occurs before phagocytosis, one of the hypotheses proposed for the pathogenesis of lesions occurring in humans with multiple sclerosis.

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