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Review
. 2019 Jul;5(7):393-396.
doi: 10.1016/j.trecan.2019.05.006. Epub 2019 Jun 4.

Glioma EVs Contribute to Immune Privilege in the Brain

Erik R Abels  1 , Marike L D Broekman  2 , Xandra O Breakefield  1 , Sybren L N Maas  3
Affiliations
Review

Glioma EVs Contribute to Immune Privilege in the Brain

Erik R Abels et al. Trends Cancer. 2019 Jul.

Abstract

Glioblastoma cells release extracellular vesicles (EVs), sometimes referred to as microvesicles and exosomes, to transfer immune modulating molecules to immune cells, resulting in an immune privileged microenvironment. Here we discuss the potential EV-mediated mechanisms underlying glioma immune modulation, as well as the technical difficulties in studying these interactions.

Keywords: exosomes; extracellular vesicles; glioblastoma; glioma; immunity.

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Figures

Figure 1.
Figure 1.. Extracellular Vesicles as a Mode of Intercellular Communication in Glioma Immunity.
Extracellular vesicles (EVs) can be formed by both the budding of the plasma membrane or through the fusion of a multivesicular body (MVB) with the plasma membrane. Cell–cell contact and the subsequent exchange of cellular components through nanotubes is an alternative method of (local) intercellular communication. EV uptake by a myeloid-derived innate immune cell can change its phenotype into an immune-suppressive, tumor-supportive effector cell, inhibiting T cell activation and supporting tumor growth by secretion of specific cytokines. Direct interaction between glioma EV surface programmed death-ligand 1 (PD-L1) and programmed cell death-1 (PD-1) expressed on T cells is an alternative direct method for glioma EVs to suppress the T cell response. Abbreviations: IL-6, interleukin 6; IL-10, interleukin 10; MCP-1, monocyte chemoattractant protein-1; VEGF, vascular endothelial growth factor.
See this image and copyright information in PMC

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