The Contribution of Microglia and Brain-Infiltrating Macrophages to the Pathogenesis of Neuroinflammatory and Neurodegenerative Diseases during TMEV Infection of the Central Nervous System.

The Contribution of Microglia and Brain-Infiltrating Macrophages to the Pathogenesis of Neuroinflammatory and Neurodegenerative Diseases during TMEV Infection of the Central Nervous System.
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DOI:
10.3390/v16010119
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发表时间:
2024-01-13
期刊:
Viruses
影响因子:
--
通讯作者:
DePaula-Silva AB
DePaula-Silva AB
中科院分区:
其他
文献类型:
--
作者:
DePaula-Silva AB

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嗜神经性病毒感染中枢神经系统(CNS)可诱导神经炎症,并与神经炎症和神经退行性疾病(包括多发性硬化和癫痫)的发展相关。先天性和适应性免疫应答(包括小胶质细胞、巨噬细胞以及T和B细胞)的激活虽然是CNS内有效病毒控制所必需的,但也与神经病理学相关。在健康条件下,常驻小胶质细胞在维持CNS内稳态方面发挥关键作用。然而,在病理事件期间,例如CNS病毒感染,小胶质细胞变得反应性,并且来自外周的免疫细胞浸润到脑中,破坏CNS稳态并促进疾病发展。Theiler鼠脑脊髓炎病毒(TMEV)是一种嗜神经性小核糖核酸病毒,用于两种不同的小鼠模型:TMEV诱导的脱髓鞘疾病(TMEV-IDD)和TMEV诱导的癫痫发作,分别代表多发性硬化症和癫痫的小鼠模型。这些小鼠模型极大地促进了我们对MS和病毒感染后癫痫发作/癫痫的病理生理学的理解,作为识别调节疾病发展的药理学靶向途径的关键工具。这篇综述旨在讨论嗜神经性小核糖核酸病毒感染过程中宿主-病原体的相互作用,并阐明我们目前对小胶质细胞和巨噬细胞在这两种复杂病毒诱导的疾病中所起的多方面作用的理解。
The infection of the central nervous system (CNS) with neurotropic viruses induces neuroinflammation and is associated with the development of neuroinflammatory and neurodegenerative diseases, including multiple sclerosis and epilepsy. The activation of the innate and adaptive immune response, including microglial, macrophages, and T and B cells, while required for efficient viral control within the CNS, is also associated with neuropathology. Under healthy conditions, resident microglia play a pivotal role in maintaining CNS homeostasis. However, during pathological events, such as CNS viral infection, microglia become reactive, and immune cells from the periphery infiltrate into the brain, disrupting CNS homeostasis and contributing to disease development. Theiler’s murine encephalomyelitis virus (TMEV), a neurotropic picornavirus, is used in two distinct mouse models: TMEV-induced demyelination disease (TMEV-IDD) and TMEV-induced seizures, representing mouse models of multiple sclerosis and epilepsy, respectively. These murine models have contributed substantially to our understanding of the pathophysiology of MS and seizures/epilepsy following viral infection, serving as critical tools for identifying pharmacological targetable pathways to modulate disease development. This review aims to discuss the host–pathogen interaction during a neurotropic picornavirus infection and to shed light on our current understanding of the multifaceted roles played by microglia and macrophages in the context of these two complexes viral-induced disease.
耦合的增殖和凋亡维持成人大脑中小胶质细胞的快速离职。
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