Complement in Neurologic Disease.

IF 28.4 1区 医学 Q1 PATHOLOGY Annual Review of Pathology-Mechanisms of Disease Pub Date : 2021-01-24 Epub Date: 2020-11-24 DOI:10.1146/annurev-pathol-031620-113409
Nicholas E Propson, Manasee Gedam, Hui Zheng
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引用次数: 20

Abstract

Classic innate immune signaling pathways provide most of the immune response in the brain. This response activates many of the canonical signaling mechanisms identified in peripheral immune cells, despite their relative absence in this immune-privileged tissue. Studies over the past decade have strongly linked complement protein production and activation to age-related functional changes and neurodegeneration. The reactivation of the complement signaling pathway in aging and disease has opened new avenues for understanding brain aging and neurological disease pathogenesis and has implicated cell types such as astrocytes, microglia, endothelial cells, oligodendrocytes, neurons, and even peripheral immune cells in these processes. In this review, we aim to unravel the past decade of research related to complement activation and its numerous consequences in aging and neurological disease.

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神经系统疾病中的补体。
经典的先天免疫信号通路提供了大脑中大部分的免疫反应。这种反应激活了外周免疫细胞中发现的许多典型信号机制,尽管它们在这种免疫特权组织中相对缺乏。过去十年的研究已经将补体蛋白的产生和激活与年龄相关的功能变化和神经变性紧密联系起来。补体信号通路在衰老和疾病中的重新激活为理解脑衰老和神经系统疾病的发病机制开辟了新的途径,并涉及星形胶质细胞、小胶质细胞、内皮细胞、少突胶质细胞、神经元甚至外周免疫细胞等细胞类型。在这篇综述中,我们旨在揭示过去十年与补体激活相关的研究及其在衰老和神经系统疾病中的众多影响。
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来源期刊
CiteScore
62.60
自引率
0.00%
发文量
40
期刊介绍: The Annual Review of Pathology: Mechanisms of Disease is a scholarly journal that has been published since 2006. Its primary focus is to provide a comprehensive overview of recent advancements in our knowledge of the causes and development of significant human diseases. The journal places particular emphasis on exploring the current and evolving concepts of disease pathogenesis, as well as the molecular genetic and morphological changes associated with various diseases. Additionally, the journal addresses the clinical significance of these findings. In order to increase accessibility and promote the broad dissemination of research, the current volume of the journal has transitioned from a gated subscription model to an open access format. This change has been made possible through the Annual Reviews' Subscribe to Open program, which allows all articles published in this volume to be freely accessible to readers. As part of this transition, all articles in the journal are published under a Creative Commons Attribution (CC BY) license, which encourages open sharing and use of the research.
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