摘要
多发性硬化(MS)是一种免疫介导中枢神经系统脱髓鞘疾病(中枢神经系统)。免疫细胞病理学女士的重要性是由临床数据连接T细胞和B细胞的损耗,或迁移进入大脑的预防显著减少复发和发展新的病变。体外研究、临床前动物模型和令人鼓舞的数据与anti-IL-17A抗体secukinumab小概念验证研究,表明,IL-17A关键白介素与许多炎症和自身免疫性疾病,可能参与女士不仅参与适应性免疫反应细胞如Th17细胞和细胞毒性T细胞,或先天免疫反应如mucosa-associated不变的T细胞和γδT细胞(MAIT),中枢神经系统也居民细胞如星形胶质细胞和少突胶质细胞可能导致当地IL-17A的生产。IL-17A加强与其他促炎细胞因子,诱导其他细胞因子的释放,介质的组织损伤和趋化因子,招募新的炎症细胞。IL-17A小胶质细胞的功能造成不利影响,星形胶质细胞,少突胶质细胞、神经元,神经细胞和内皮细胞前体。封锁IL-17A可能有利于医学患者不仅通过抑制炎症和组织破坏,而且还通过提高修复过程。
关键词: IL-17、IL17RA IL-17RC
图形摘要
Current Drug Targets
Title:IL-17A and Multiple Sclerosis: Signaling Pathways, Producing Cells and Target Cells in the Central Nervous System
Volume: 17 Issue: 16
Author(s): Frank Kolbinger, Christine Huppertz, Anis Mir, Franco Di Padova
Affiliation:
关键词: IL-17、IL17RA IL-17RC
摘要: Multiple sclerosis (MS) is an immune mediated demyelinating disease of the central nervous system (CNS). The importance of immune cells to MS pathology is supported by clinical data linking the depletion of T and B cells, or the prevention of their migration into the brain with significant reduction in relapses and development of new lesions. In vitro studies, preclinical animal models and encouraging data with the anti-IL-17A antibody secukinumab in a small proof of concept study in man, indicate that IL-17A, a key interleukin associated with many inflammatory and autoimmune diseases, may be involved in MS. Not only cells involved in adaptive immune responses such as Th17 cells and cytotoxic T cells, or innate immune responses such as mucosa-associated invariant T (MAIT) cells and γδT cells, but also CNS resident cells such as astrocytes and oligodendrocytes might contribute to the local production of IL-17A. IL-17A synergizes with other proinflammatory cytokines, by inducing the release of additional cytokines, mediators of tissue damage and chemokines, that recruit new inflammatory cells. IL-17A adversely affects the functions of microglia, astrocytes, oligodendrocytes, neurons, neural precursor cells and endothelial cells. Blockade of IL-17A might be beneficial to MS patients not only by inhibiting inflammation and tissue destruction, but also by enhancing repair processes.
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Cite this article as:
Frank Kolbinger, Christine Huppertz, Anis Mir, Franco Di Padova , IL-17A and Multiple Sclerosis: Signaling Pathways, Producing Cells and Target Cells in the Central Nervous System, Current Drug Targets 2016; 17 (16) . https://dx.doi.org/10.2174/1389450117666160307144027
DOI https://dx.doi.org/10.2174/1389450117666160307144027 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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