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脱髓鞘伴少突胶质细胞营养不良:多发性硬化石蜡块的复杂信息。

Demyelination with preferential MAG loss: A complex message from MS paraffin blocks.

机构信息

MS Research Center, Neuroscience Institute, Tehran University of Medical Science, Tehran, Iran.

Department of Neurology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA.

出版信息

J Neurol Sci. 2018 Feb 15;385:126-130. doi: 10.1016/j.jns.2017.12.029. Epub 2017 Dec 24.

Abstract

Multiple sclerosis (MS) is generally considered to be a demyelinating autoimmune disorder. However, neuropathological examinations of MS lesions do not support this concept. Demyelination with preferential loss of myelin-associated glycoprotein (MAG) is a common finding in MS tissues and has been reported by several groups. As MAG is located in ad-axonal myelin layers and is not accessible to infiltrating immune cells, demyelination with preferred loss of MAG may be suggestive of a primary oligodendrocytopathy in MS. Moreover, it has been shown that oligodendrocytopathy may precede the infiltration of inflammatory cells at the lesion site. In this paper, we review studies of neuropathology of MS tissues that reported this type of demyelination and then we discuss three emerging explanations that are trying to interpret this mismatched observation.

摘要

多发性硬化症(MS)通常被认为是一种脱髓鞘自身免疫性疾病。然而,对 MS 病变的神经病理学检查并不支持这一概念。脱髓鞘伴髓鞘相关糖蛋白(MAG)优先丢失是 MS 组织中的常见发现,已有多个研究小组报道过。由于 MAG 位于轴突旁髓鞘层,浸润的免疫细胞无法接触到它,因此 MAG 优先丢失的脱髓鞘可能提示 MS 中的原发性少突胶质细胞病。此外,已经表明少突胶质细胞病可能先于病变部位炎症细胞的浸润。在本文中,我们回顾了报道这种脱髓鞘类型的 MS 组织神经病理学研究,然后讨论了三种试图解释这种不匹配观察结果的新兴解释。

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