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. 2022 Feb 19;41:68. doi: 10.1186/s13046-022-02272-x

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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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — A Schematic illustration of PNP@R@M-T developed for efficient and selective reprogramming of M2-like macrophages and enhanced cancer immunotherapy via M2pep-mediated endocytosis. B-F Inhibitory effects of PNP@R@M-T on tumor growth in vivo. B Schematic illustration of induction and treatment of B16-OVA tumors in C57BL/6 mice. C Body weights of mice treated with PBS, R848, PNP@R, PNP@R@M-S, and PNP@R@M-T. D The survival rate was analyzed by the log-rank test (n = 10 mice). E B16-OVA tumor growth. n = 6 mice. F Macroscopic images of tumors taken 18 days after the initiation of treatment. Representative images from 6 mice per group are shown [28]