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Published on: April 13, 2017
Roles and regulation of microglia activity in multiple sclerosis: insights from animal models
Félix Distéfano-Gagné1,2, Sara Bitarafan1,2, Steve Lacroix1,2
1Axe Neuroscience, Centre de Recherche du CHU de Québec - Université Laval, Québec, Québec, Canada.
Abstract:
As resident macrophages of the CNS, microglia are critical immune effectors of inflammatory lesions and associated neural dysfunctions. In multiple sclerosis (MS) and its animal models, chronic microglial inflammatory activity damages myelin and disrupts axonal and synaptic activity. In contrast to these detrimental effects, the potent phagocytic and tissue-remodelling capabilities of microglia support critical endogenous repair mechanisms. Although these opposing capabilities have long been appreciated, a precise understanding of their underlying molecular effectors is only beginning to emerge. Here, we review recent advances in our understanding of the roles of microglia in animal models of MS and demyelinating lesions and the mechanisms that underlie their damaging and repairing activities. We also discuss how the structured organization and regulation of the genome enables complex transcriptional heterogeneity within the microglial cell population at demyelinating lesions.
Insights
Microglia, the CNS immune cells, have dual roles in multiple sclerosis (MS) models, causing damage but also aiding repair. Understanding their molecular mechanisms is key to developing new therapies for demyelinating lesions.
Area of Science:
- Neuroimmunology
- Cellular Biology
Background:
- Microglia are the resident macrophages of the central nervous system (CNS).
- In multiple sclerosis (MS) and animal models, chronic microglial activation contributes to myelin damage and neural dysfunction.
- Microglia also possess phagocytic and tissue-remodeling capabilities crucial for endogenous repair.
Purpose of the Study:
- To review recent advances in understanding microglial roles in MS and demyelinating lesions.
- To elucidate the molecular mechanisms underlying microglial damaging and repairing activities.
- To discuss the impact of genome regulation on microglial transcriptional heterogeneity.
Main Methods:
- Literature review of recent advances in microglial research in MS models.
- Analysis of molecular mechanisms of microglial function in demyelination.
- Discussion of genomic regulation and transcriptional heterogeneity.
Main Results:
- Microglia exhibit both detrimental inflammatory and beneficial repair functions in demyelinating diseases.
- Specific molecular effectors driving these opposing functions are beginning to be identified.
- Genome organization and regulation contribute to diverse microglial phenotypes at lesion sites.
Conclusions:
- Microglial functions in MS are complex, involving both pathology and repair.
- Further research into microglial molecular mechanisms is essential for therapeutic development.
- Transcriptional heterogeneity in microglia at lesions is influenced by genomic regulation.
