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. 2017 Dec 14;37(9):1175–1191. doi: 10.1038/s41388-017-0034-x

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© The Author(s) 2017

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Internalization and proliferation in response to TEC-derived EVs and anti-IL-3R-EVs. a Number of EV particles (mean ± SD) was calculated per ml. Data refer to EV-derived from untreated TECs (EVs) or anti-IL-3Rα blocking antibody-treated TECs (anti-IL-3R-EVs) (n = 4, unpaired t-test). b Representative images of NanoSight analyses performed on the 100 k fraction of TEC-derived EVs, showing a mean dimension, for both EVs, of 169 nm (n = 3). c TEC-derived EVs were analyzed for CD63 and CD81 exosomal markers by western blot analysis (n = 4, unpaired t-test). d Representative confocal microscopy images of TECs, either untreated or treated for 3 h with the indicated PKH26-labeled EVs, to evaluate EV up-take TECs. (n = 4). Scale bars indicate 10 μm (40× magnification). e Cell proliferation assay was performed in TECs untreated (none) or treated for 24 h with EVs or anti-IL-3R-EVs and reported as number of cells per field (mean ± SD, 20× magnification) (n = 5) (***p < 0.001, none vs EVs; ***p < 0.001, none and EVs vs anti-IL-3R-EVs, one-way ANOVA). f TECs, either alone or stimulated with EVs or anti-IL-3R-EVs, were lysed and analyzed for cyclin D1 content. Protein levels were normalized to β-actin content (**p < 0.01, none vs anti-IL-3R-EVs; ***p < 0.001, EVs vs anti-IL-3R-EVs, one-way ANOVA) (n = 4)