揭示多发性硬化症的免疫发病机制:质母细胞和致病T细胞的动态舞蹈

Yasunari Matsuzaka, Ryu Yashiro
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摘要

多发性硬化症(MS)是一种慢性中枢神经系统炎症性脱髓鞘疾病,其特征是在时间和空间上发生多发性病变。此外,多发性硬化症是一种在白人人群中占主导地位的疾病。近年来,患者数量迅速增加,多见于年轻人,平均发病年龄在30岁左右,但也可发生在儿童和老年人身上。女性比男性更常见,男女比例约为1:3。作为MS的免疫发病机制,一组被称为浆母细胞的B细胞通过产生IL-10来控制脑脊髓炎。这些产生il -10的B细胞,被称为调节性B细胞,在包括ms在内的自身免疫性疾病的实验小鼠模型中抑制炎症反应。由于已经明确这些调节性B细胞是质母细胞,预计在外周血中cd8阳性T细胞中,人工控制质母细胞分化将导致ms的新治疗方法的发展。与健康对照相比,MS患者的pd -1阳性细胞比例降低。抑制受体在T细胞上表达的功能障碍是MS免疫病理的核心,可能是慢性持续性炎症的原因。PD-1+ CD8+ T细胞在ms等其他免疫性神经疾病中也可以作为反映每个患者病情的指标,Th17细胞还调节包括ms在内的各种自身免疫性疾病的发展,因此,恢复减弱的免疫调节功能可能是一种真正的疾病修饰治疗。到目前为止,类固醇和免疫抑制剂一直是治疗自身免疫性疾病的主流药物,但问题是,这不仅会杀死致病性T细胞,还会杀死人体所必需的淋巴细胞。从对MS免疫调节的理解出发,我们可以期待只针对致病免疫细胞的治疗策略的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Unraveling the Immunopathogenesis of Multiple Sclerosis: The Dynamic Dance of Plasmablasts and Pathogenic T Cells
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system, characterized by multiple lesions occurring temporally and spatially. Additionally, MS is a disease that predominates in the white population. In recent years, there has been a rapid increase in the number of patients, and it often occurs in young people, with an average age of onset of around 30 years old, but it can also occur in children and the elderly. It is more common in women than men, with a male-to-female ratio of approximately 1:3. As the immunopathogenesis of MS, a group of B cells called plasmablasts controls encephalomyelitis via IL-10 production. These IL-10-producing B cells, called regulatory B cells, suppress inflammatory responses in experimental mouse models of autoimmune diseases including MS. Since it has been clarified that these regulatory B cells are plasmablasts, it is expected that the artificial control of plasmablast differentiation will lead to the development of new treatments for MS. Among CD8-positive T cells in the peripheral blood, the proportion of PD-1-positive cells is decreased in MS patients compared with healthy controls. The dysfunction of inhibitory receptors expressed on T cells is known to be the core of MS immunopathology and may be the cause of chronic persistent inflammation. The PD-1+ CD8+ T cells may also serve as indicators that reflect the condition of each patient in other immunological neurological diseases such as MS. Th17 cells also regulate the development of various autoimmune diseases, including MS. Thus, the restoration of weakened immune regulatory functions may be a true disease-modifying treatment. So far, steroids and immunosuppressants have been the mainstream for autoimmune diseases, but the problem is that this kills not only pathogenic T cells, but also lymphocytes, which are necessary for the body. From this understanding of the immune regulation of MS, we can expect the development of therapeutic strategies that target only pathogenic immune cells.
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