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. 2022 Apr 8;392(1):247–267. doi: 10.1007/s00441-022-03621-0

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Schematic diagram showing extracellular vesicle (EV) generation and pathogenic prion protein (PrP^TSE) localisation in EVs. Small EVs (exosomes; < 200 nm) are generated via endosomal pathways when the multivesicular bodies (MVBs) fuse with the plasma membrane. These carry several classes of marker protein including tetraspanins, endosomal sorting complex required for transport (ESCRT) proteins, neutral sphingomyelinase 2 (nSMase2), heat shock proteins (HSPs) and integrins as defined in the Minimal Information for Studies of Extracellular Vesicles (MISEV) guidelines (Théry et al. 2018). Microvesicles are generated via blebbing or shedding from the plasma membrane, and apoptotic bodies are generated via cellular fragmentation in cells undergoing apoptotic cell death. Studies have demonstrated PrP^TSE localisation in the plasma membrane, endolysosomal system including the endoplasmic reticulum (ER), and EVs