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Updated: Jul 9, 2025
Characterization of Immune Cell-derived Extracellular Vesicles and Studying Functional Impact on Cell Environment
Published on: June 2, 2020
Microglia-derived extracellular vesicles in homeostasis and demyelination/remyelination processes
V S B Wies Mancini1,2, V S Mattera1,2, J M Pasquini1,2
1Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Cátedra de Química Biológica Patológica, Universidad de Buenos Aires, Buenos Aires, Argentina.
Abstract:
Microglia (MG) play a crucial role as the predominant myeloid cells in the central nervous system and are commonly activated in multiple sclerosis. They perform essential functions under normal conditions, such as actively surveying the surrounding parenchyma, facilitating synaptic remodeling, engulfing dead cells and debris, and protecting the brain against infectious pathogens and harmful self-proteins. Extracellular vesicles (EVs) are diverse structures enclosed by a lipid bilayer that originate from intracellular endocytic trafficking or the plasma membrane. They are released by cells into the extracellular space and can be found in various bodily fluids. EVs have recently emerged as a communication mechanism between cells, enabling the transfer of functional proteins, lipids, different RNA species, and even fragments of DNA from donor cells. MG act as both source and recipient of EVs. Consequently, MG-derived EVs are involved in regulating synapse development and maintaining homeostasis. These EVs also directly influence astrocytes, significantly increasing the release of inflammatory cytokines like IL-1β, IL-6, and TNF-α, resulting in a robust inflammatory response. Furthermore, EVs derived from inflammatory MG have been found to inhibit remyelination, whereas Evs produced by pro-regenerative MG effectively promote myelin repair. This review aims to provide an overview of the current understanding of MG-derived Evs, their impact on neighboring cells, and the cellular microenvironment in normal conditions and pathological states, specifically focusing on demyelination and remyelination processes.
Insights
Microglia-derived extracellular vesicles (EVs) are key communicators in the brain, influencing inflammation and myelin repair in conditions like multiple sclerosis. Understanding these EVs is vital for neurological health.
Area of Science:
- Neuroscience
- Cell Biology
- Immunology
Background:
- Microglia (MG) are the primary immune cells in the central nervous system, crucial for brain homeostasis and disease states.
- Extracellular vesicles (EVs) are lipid-bound structures released by cells, mediating intercellular communication through cargo transfer.
- Microglia are both producers and receivers of EVs, highlighting their role in cell-to-cell signaling within the brain.
Purpose of the Study:
- To review the current understanding of microglia-derived EVs.
- To explore the impact of these EVs on neighboring cells and the microenvironment.
- To focus on the role of microglia-derived EVs in demyelination and remyelination processes, particularly in multiple sclerosis.
Main Methods:
- Literature review of studies on microglia and extracellular vesicles.
- Analysis of research on EV-mediated communication in the central nervous system.
- Synthesis of findings related to MG-EVs in physiological and pathological conditions, including demyelination and remyelination.
Main Results:
- Microglia-derived EVs regulate synaptic development and maintain brain homeostasis.
- These EVs can induce inflammatory responses by stimulating astrocytes to release cytokines (IL-1β, IL-6, TNF-α).
- EVs from inflammatory microglia inhibit remyelination, while those from pro-regenerative microglia promote myelin repair.
Conclusions:
- Microglia-derived EVs are critical mediators of cellular interactions and microenvironmental regulation in the brain.
- Dysfunctional microglia-derived EVs contribute to inflammatory processes and hinder myelin repair in demyelinating diseases.
- Further research into MG-EVs offers potential therapeutic avenues for neurological disorders affecting myelin.
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