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多发性硬化症:抗体和补体介导的脱髓鞘的原位证据。

Multiple sclerosis: in situ evidence for antibody- and complement-mediated demyelination.

作者信息

Storch M K, Piddlesden S, Haltia M, Iivanainen M, Morgan P, Lassmann H

机构信息

Institute of Neurology, University of Vienna, Wien, Austria.

出版信息

Ann Neurol. 1998 Apr;43(4):465-71. doi: 10.1002/ana.410430409.

DOI:10.1002/ana.410430409
PMID:9546327
Abstract

We describe a case of multiple sclerosis characterized by deposition of immunoglobulin and complement in the areas of active demyelination. This was particularly evident for the C9neo antigen, which is a marker for the activated lytic complement complex and was exclusively deposited in the areas of active myelin destruction. In addition, macrophages in the lesions contained degradation products that were immunoreactive for myelin antigens, immunoglobulins, and C9neo antigen. Destruction of myelin sheaths was associated with incomplete loss of oligodendrocytes in the active areas and reappearance of oligodendrocytes with remyelination in the inactive plaque center.

摘要

我们描述了一例多发性硬化症病例,其特征为免疫球蛋白和补体在活跃脱髓鞘区域沉积。这在C9neo抗原方面尤为明显,C9neo抗原是活化溶解性补体复合物的标志物,且仅沉积于活跃的髓鞘破坏区域。此外,病变中的巨噬细胞含有对髓鞘抗原、免疫球蛋白和C9neo抗原呈免疫反应性的降解产物。髓鞘的破坏与活跃区域少突胶质细胞的不完全丧失以及非活跃斑块中心再髓鞘化时少突胶质细胞的重新出现有关。

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