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. 2022 Jun 29;5:633. doi: 10.1038/s42003-022-03569-5

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© The Author(s) 2022

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. 8 — Samples were stained with CFDA-SE and anti-human and anti-mouse CD31 (conjugated to BV421 and APC, respectively). Quantification of (a) CFSE + anti-human CD31 + single EV ≤ 400 nm showed a linear increase corresponding to the increase in human PPP abundance (R² = 0.95), while (b) CFSE + anti-mouse CD31 + single EV ≤ 400 nm showed a linear decrease corresponding to the decrease in mouse PPP abundance (R² = 0.81). Data were obtained through three independent experiments using the same human and mouse PPP samples. X-axis: v/v ratio of mouse – human PPP. Data shown represent the mean ± standard error. Red dashed lines: background concentrations of our protocol as indicated by the measurement of isotype controls.