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:
影响因子:
--
通讯作者:
DePaula-Silva AB
中科院分区:
文献类型:
--
作者:
DePaula-Silva AB
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.
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影响因子:
8.8
作者:
Askew K;Li K;Olmos-Alonso A;Garcia-Moreno F;Liang Y;Richardson P;Tipton T;Chapman MA;Riecken K;Beccari S;Sierra A;Molnár Z;Cragg MS;Garaschuk O;Perry VH;Gomez-Nicola D
通讯作者:
Gomez-Nicola D
DOI:
10.1111/febs.15428
发表时间:
2020-11
期刊:
The FEBS journal
影响因子:
--
作者:
Bosco DB;Tian DS;Wu LJ
通讯作者:
Wu LJ
影响因子:
5.6
作者:
Brandenburg S;Blank A;Bungert AD;Vajkoczy P
通讯作者:
Vajkoczy P
影响因子:
64.8
作者:
通讯作者:
--
影响因子:
--
作者:
Ahadiat SAA;Hosseinian Z
通讯作者:
Hosseinian Z