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. Author manuscript; available in PMC: 2021 Jun 28.
Published in final edited form as: Trends Cancer. 2019 Jun 4;5(7):393–396. doi: 10.1016/j.trecan.2019.05.006

Figure 1. Extracellular Vesicles as a Mode of Intercellular Communication in Glioma Immunity.

Figure 1.

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.