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. 2018 Jul 30;17:108. doi: 10.1186/s12943-018-0858-1

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 1 — Development of the pancreatic cancer microenvironment. Pancreatic cancer cells secrete cytokines and chemokines to recruit or activate stromal cells for desmoplasia and immune evasion, including myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), regulatory T cells (Tregs), and pancreatic stellate cells (PSCs). Among them, PSCs are the main source of ECM deposition, and the TAM-PSC axis can facilitate desmoplasia. These cells within the pancreatic cancer microenvironment can help pancreatic cancer cells inhibit CD8⁺ T cells to overcome the immune surveillance by expressing or producing various factors, such as IL-10, TGFβ, PD-L1, and IDO