Microglial cells represent the resident immune elements of the central nervous system, where they exert constant monitoring and contribute to preserving neuronal activity and function. In the context of glioblastoma (GBM), a common type of tumor originating in the brain, microglial cells deeply modify their phenotype, lose their homeostatic functions, invade the tumoral mass and support the growth and further invasion of the tumoral cells into the surrounding brain parenchyma. These modifications are, at least in part, induced by bidirectional communication among microglial and tumoral cells through the release of soluble molecules and extracellular vesicles (EVs). EVs produced by GBM and microglial cells transfer different kinds of biological information to receiving cells, deeply modifying their phenotype and activity and could represent important diagnostic markers and therapeutic targets. Recent evidence demonstrates that in GBM, microglial-derived EVs contribute to the immune suppression of the tumor microenvironment (TME), thus favoring GBM immune escape. In this review, we report the current knowledge on EV formation, biogenesis, cargo and functions, with a focus on the effects of microglia-derived EVs in GBM. What clearly emerges from this analysis is that we are at the beginning of a full understanding of the complete picture of the biological effects of microglial-derived EVs and that further investigations using multidisciplinary approaches are necessary to validate their use in GBM diagnosis and therapy.

Microglial Extracellular Vesicles as Modulators of Brain Microenvironment in Glioma / Catalano, Myriam; Serpe, Carmela; Limatola, Cristina. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1422-0067. - 23:21(2022), p. 13165. [10.3390/ijms232113165]

Microglial Extracellular Vesicles as Modulators of Brain Microenvironment in Glioma

Myriam Catalano
Primo
Conceptualization
;
Carmela Serpe
Methodology
;
Cristina Limatola
Ultimo
Supervision
2022

Abstract

Microglial cells represent the resident immune elements of the central nervous system, where they exert constant monitoring and contribute to preserving neuronal activity and function. In the context of glioblastoma (GBM), a common type of tumor originating in the brain, microglial cells deeply modify their phenotype, lose their homeostatic functions, invade the tumoral mass and support the growth and further invasion of the tumoral cells into the surrounding brain parenchyma. These modifications are, at least in part, induced by bidirectional communication among microglial and tumoral cells through the release of soluble molecules and extracellular vesicles (EVs). EVs produced by GBM and microglial cells transfer different kinds of biological information to receiving cells, deeply modifying their phenotype and activity and could represent important diagnostic markers and therapeutic targets. Recent evidence demonstrates that in GBM, microglial-derived EVs contribute to the immune suppression of the tumor microenvironment (TME), thus favoring GBM immune escape. In this review, we report the current knowledge on EV formation, biogenesis, cargo and functions, with a focus on the effects of microglia-derived EVs in GBM. What clearly emerges from this analysis is that we are at the beginning of a full understanding of the complete picture of the biological effects of microglial-derived EVs and that further investigations using multidisciplinary approaches are necessary to validate their use in GBM diagnosis and therapy.
2022
CNS; extracellular vesicles; glioma; immune evasion; microglia; Humans; Microglia; Cell Line, Tumor; Tumor Microenvironment; Brain; Brain Neoplasms; Glioblastoma; Extracellular Vesicles
01 Pubblicazione su rivista::01g Articolo di rassegna (Review)
Microglial Extracellular Vesicles as Modulators of Brain Microenvironment in Glioma / Catalano, Myriam; Serpe, Carmela; Limatola, Cristina. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1422-0067. - 23:21(2022), p. 13165. [10.3390/ijms232113165]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1661054
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