小胶质细胞与多发性硬化症

Q3 Neuroscience
Brady P Hammond, Sharmistha P Panda, Deepak K Kaushik, Jason R Plemel
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引用次数: 0

摘要

多发性硬化症(MS)是一种毁灭性的自身免疫性疾病,会导致严重残疾。这种残疾源于中枢神经系统(CNS)中随机的、区域性的髓鞘(神经元周围的绝缘鞘)脱落。脱髓鞘区域主要由大脑中的巨噬细胞--小胶质细胞--占据。小胶质细胞在多发性硬化症中发挥着多种功能,人们认为它们通过与进入大脑的外周免疫细胞相互作用,启动并延续脱髓鞘。然而,小胶质细胞也可能是招募和促进细胞分化的关键,这些细胞可以在称为再髓鞘化的过程中恢复丢失的髓鞘。鉴于这些看似相反的功能,这些免疫细胞究竟是有益还是有害尚无定论。在本章中,我们将讨论小胶质细胞在整个多发性硬化症病程中的动态变化,并探讨小胶质细胞作为脱髓鞘和再髓鞘化的驱动因素这一明显的二分法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Microglia and Multiple Sclerosis.

Multiple sclerosis (MS) is a devastating autoimmune disease that leads to profound disability. This disability arises from the stochastic, regional loss of myelin-the insulating sheath surrounding neurons-in the central nervous system (CNS). The demyelinated regions are dominated by the brain's resident macrophages: microglia. Microglia perform a variety of functions in MS and are thought to initiate and perpetuate demyelination through their interactions with peripheral immune cells that traffic into the brain. However, microglia are also likely essential for recruiting and promoting the differentiation of cells that can restore lost myelin in a process known as remyelination. Given these seemingly opposing functions, an overarching beneficial or detrimental role is yet to be ascribed to these immune cells. In this chapter, we will discuss microglia dynamics throughout the MS disease course and probe the apparent dichotomy of microglia as the drivers of both demyelination and remyelination.

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来源期刊
Advances in neurobiology
Advances in neurobiology Neuroscience-Neurology
CiteScore
2.80
自引率
0.00%
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