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首页> 外文期刊>Journal of neurology >The pathology of multiple sclerosis is the result of focal inflammatory demyelination with axonal damage.
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The pathology of multiple sclerosis is the result of focal inflammatory demyelination with axonal damage.

机译：多发性硬化的病理学是局部炎性脱髓鞘与轴突损伤的结果。

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Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system manifested morphologically by inflammation, demyelination, axonal loss and gliosis. The inflammatory lesions are characterized by massive infiltration by a heterogeneous population of cellular and soluble mediators of the immune system, including T cells, B cells, macrophages and mi croglia, as well as a broad range of cytokines, chemokines, antibodies, complement and other toxic substances. The appearance of such lesions is associated with clinical relapses. Recent detailed immunopathological studies of early, acute lesions revealed profound heterogeneity in the patterns of demyelination and the factors of the immune system involved. During remission, resolution of inflammation is the main factor which leads to clinical improvement of patients. However, the immune system can play a beneficial role at this stage, promoting remyelination perhaps by production of growth factors such as BDNF. In contrast, the progressive irreversible neurological deficit in multiple sclerosis is associated with neurodegenerative processes resulting in axonal and neuronal loss. The mechanisms behind damage to axons in multiple sclerosis lesions are poorly understood. However, the close proximity of areas with prominent axonal loss and areas containing inflammatory infiltrates (e. g., T cells, macrophages) suggest that axonal damage is closely associated with inflammation. Different soluble or cellular mediators of the immune response have been shown to damage axons in experimental systems, and these may be responsible for neurodegeneration in human disease.
机译：多发性硬化症是中枢神经系统的慢性炎症性脱髓鞘疾病，其形态学表现为炎症，脱髓鞘，轴突丢失和神经胶质增生。炎性病变的特征是免疫系统的细胞和可溶性介导物的异质群体大量浸润，包括T细胞，B细胞，巨噬细胞和绒毛膜，以及广泛的细胞因子，趋化因子，抗体，补体和其他有毒物质。这种病变的出现与临床复发有关。最近对早期，急性病变的详细免疫病理学研究表明，脱髓鞘的模式和所涉及的免疫系统的因素存在巨大的异质性。在缓解期间，炎症的消除是导致患者临床改善的主要因素。但是，免疫系统在此阶段可以发挥有益作用，可能通过产生生长因子（如BDNF）来促进髓鞘再生。相反，多发性硬化中进行性不可逆的神经功能缺损与导致轴突和神经元丢失的神经退行性过程相关。对多发性硬化病变中轴突损伤背后的机制了解甚少。但是，轴突损失明显的区域和含有炎性浸润物的区域（例如，T细胞，巨噬细胞）的近距离表明轴突损伤与炎症密切相关。已显示免疫反应的不同可溶性或细胞介体会破坏实验系统中的轴突，而这些轴突可能是人类疾病中神经变性的原因。

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