Alpha-Synuclein Induced Immune Cells Activation and Associated Therapy in Parkinson's Disease.

Alpha-Synuclein Induced Immune Cells Activation and Associated Therapy in Parkinson's Disease.
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α-突触核蛋白诱导免疫细胞激活及帕金森病的相关治疗。

DOI:
10.3389/fnagi.2021.769506
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发表时间:
2021
影响因子:
4.8
通讯作者:
Zhou T
Zhou T
中科院分区:
医学2区
文献类型:
--
作者:
Su R;Zhou T

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帕金森病是一种与免疫密切相关的神经退行性疾病。PD发病机制的一个重要方面是α-突触核蛋白与一系列免疫细胞之间的相互作用。研究表明,α-突触核蛋白的积累可诱导加速PD进展的自身免疫反应。本研究探讨了α-突触核蛋白与免疫系统相互作用的机制。在PD的发展过程中,异常积累的α-突触核蛋白成为一种自身免疫抗原,与Toll样受体(TLR)结合,激活小胶质细胞,从而分化为小胶质细胞1型(M1)亚型。小胶质细胞激活细胞内炎症通路,诱导促炎细胞因子的释放,并促进分化簇4 +(CD 4+)T细胞分化为促炎性辅助性T细胞1型(Th 1)和辅助性T细胞17型(Th 17)亚型。鉴于α-突触核蛋白在PD患者免疫系统中的重要作用,确定与α-突触核蛋白相关的免疫治疗的潜在靶点对于减缓疾病进展至关重要。对PD免疫相关机制的深入了解可以指导未来相关治疗策略的发展。
Parkinson’s disease (PD) is a neurodegenerative disorder closely related to immunity. An important aspect of the pathogenesis of PD is the interaction between α-synuclein and a series of immune cells. Studies have shown that accumulation of α-synuclein can induce an autoimmune response that accelerates the progression of PD. This study discusses the mechanisms underlying the interaction between α-synuclein and the immune system. During the development of PD, abnormally accumulated α-synuclein becomes an autoimmune antigen that binds to Toll-like receptors (TLRs) that activate microglia, which differentiate into the microglia type 1 (M1) subtype. The microglia activate intracellular inflammatory pathways, induce the release of proinflammatory cytokines, and promote the differentiation of cluster of differentiation 4 + (CD4 +) T cells into proinflammatory T helper type 1 (Th1) and T helper type 17 (Th17) subtypes. Given the important role of α-synuclein in the immune system of the patients with PD, identifying potential targets of immunotherapy related to α-synuclein is critical for slowing disease progression. An enhanced understanding of immune-associated mechanisms in PD can guide the development of associated therapeutic strategies in the future.
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发表时间: 2020-12
影响因子: 6.1
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影响因子: 3.3
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