自身免疫过程在神经系统脱髓鞘疾病中的作用:聚焦多发性硬化症

F. Hladkykh
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引用次数: 0

摘要

背景。中枢神经系统(CNS)脱髓鞘疾病是一类以神经细胞轴突髓鞘受损为特征的异质性疾病。多发性硬化症(MS)是中枢神经系统最常见的慢性炎症性脱髓鞘疾病,影响着全球 290 多万人。本研究的目的是根据公开信息来源的数据,总结目前有关多发性硬化症免疫发病机制特征的信息。材料和方法。使用以下关键词在 PubMed、Clinical Key Elsevier、Cochrane Library、eBook Business Collection 和 Google Scholar 数据库中筛选涉及多发性硬化症免疫发病机制特征的出版物:多发性硬化症、脱髓鞘疾病、神经变性、少突胶质细胞。研究结果多发性硬化症的病程分为三个连续的阶段/形式,即复发缓解期、原发性进展期和继发性进展期。免疫机制异常被认为是多发性硬化症发病机制的主角。自反应性髓鞘特异性淋巴细胞在中枢神经系统外被激活,它们穿过血脑屏障,形成新的炎性脱髓鞘病变。在多发性硬化症的适应性免疫反应中,髓鞘化少突胶质细胞是一个靶点。进行性多发性硬化症患者脑部的炎症反应主要发生在脑膜的大结缔组织和脑室周围间隙。多发性硬化症的治疗可分为三类:急性复发治疗、疾病改变治疗和对症治疗。结论在T细胞方面,hel-per(CD4+)和细胞毒性(CD8+)T细胞都参与了多发性硬化症的中枢神经系统损伤。外周激活的 T 细胞亚群(CD4+ Th1 和 Th17,CD8+)通过血脑屏障迁移,激活 B 细胞和巨噬细胞,从而引起神经炎症反应,导致中枢神经系统脱髓鞘和神经变性。在中枢神经系统中广泛分布的少突胶质祖细胞介导髓鞘化和再髓鞘化。治疗多发性硬化症的新方法所需的特征之一是恢复抗原特异性耐受。
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The role of autoimmune processes in demyelinating diseases of the nervous system: focus on multiple sclerosis
Background. Demyelinating diseases of the central nervous system (CNS) are a heterogeneous group of disorders characterized by a damage to the myelin sheath of nerve cell axons. Multiple sclerosis (MS) is the most common chronic inflammatory demyelinating disease of the CNS affecting more than 2.9 million people worldwide. The purpose was to summarize current information about the features of the immunopathogenesis of multiple sclerosis according to the data from open sources of information. Materials and methods. The selection of publications covering the features of the immunopathogenesis of multiple sclerosis was carried out in the PubMed, Clinical Key Elsevier, Cochrane Library, eBook Business Collection and Google Scholar databases using the following keywords: multiple sclerosis, demyelinating diseases, neurodegeneration, oligodendrocytes. Results. The course of MS has three successive phases/forms known as relapsing-remitting, primary progressive and secondary progressive. Abnormalities of immune mechanisms are proposed as protagonists of the pathogenesis of MS. Autoreactive myelin-specific lymphocytes are activated outside the CNS, they cross the blood-brain barrier and form new inflammatory demyelinating lesions. The myelinating oligodendrocyte is a target during the adaptive immune response in MS. The inflammatory reaction in the brain of patients with progressive MS is observed mainly in the large connective tissues of the meninges and the periventricular space. Treatment of MS can be divided into three categories: treatment of acute relapse, disease-modifying treatment, and symptomatic treatment. Conclusions. On the T cell side, both hel-per (CD4+) and cytotoxic (CD8+) T cells are involved in the CNS damage in MS. Peripherally activated subsets of T cells (CD4+ Th1 and Th17, CD8+) migrate through the blood-brain barrier and activate B-cells and macrophages, which causes a neuroinflammatory reaction and leads to demyelination and neurodegeneration in the CNS. Oligodendrocyte progenitor cells, which are widely distributed throughout the CNS, mediate myelination and remyelination. One of the desired features of new methods for treating MS is the restoration of antigen-specific tolerance.
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