Chen Junjue, Liu Xiaohong, Zhong Yisheng
Department of Ophthalmology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Front Aging Neurosci. 2020 Sep 29;12:566922. doi: 10.3389/fnagi.2020.566922. eCollection 2020.
Neurodegenerative diseases are characterized by the loss of neurons and/or myelin sheath, which deteriorate over time and cause dysfunction. Interleukin 17A is the signature cytokine of a subset of CD4 helper T cells known as Th17 cells, and the IL-17 cytokine family contains six cytokines and five receptors. Recently, several studies have suggested a pivotal role for the interleukin-17A (IL-17A) cytokine family in human inflammatory or autoimmune diseases and neurodegenerative diseases, including psoriasis, rheumatoid arthritis (RA), Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and glaucoma. Studies in recent years have shown that the mechanism of action of IL-17A is more subtle than simply causing inflammation. Although the specific mechanism of IL-17A in neurodegenerative diseases is still controversial, it is generally accepted now that IL-17A causes diseases by activating glial cells. In this review article, we will focus on the function of IL-17A, in particular the proposed roles of IL-17A, in the pathogenesis of neurodegenerative diseases.
神经退行性疾病的特征是神经元和/或髓鞘的丧失,这些会随着时间推移而恶化并导致功能障碍。白细胞介素17A是称为Th17细胞的CD4辅助性T细胞亚群的标志性细胞因子,白细胞介素17细胞因子家族包含六种细胞因子和五种受体。最近,多项研究表明白细胞介素-17A(IL-17A)细胞因子家族在人类炎症性或自身免疫性疾病以及神经退行性疾病中起关键作用,这些疾病包括银屑病、类风湿性关节炎(RA)、阿尔茨海默病(AD)、帕金森病(PD)、多发性硬化症(MS)、肌萎缩侧索硬化症(ALS)和青光眼。近年来的研究表明,IL-17A的作用机制比单纯引发炎症更为微妙。尽管IL-17A在神经退行性疾病中的具体机制仍存在争议,但目前普遍认为IL-17A通过激活神经胶质细胞引发疾病。在这篇综述文章中,我们将重点关注IL-17A的功能,特别是IL-17A在神经退行性疾病发病机制中的作用。
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