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. 2023 Jan 4;30:1. doi: 10.1186/s12929-022-00894-z

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© The Author(s) 2023

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. 2 — CAFs modulate the immunosuppressive microenvironment. CAFs promote immune suppression and abolish immune surveillance in the TME. CAFs secrete TGFβ and CCL5 to differentiate naïve T cells into Tregs and to recruit Tregs. CCL2, IL6, and IL33 secreted by CAFs help to recruit MDSCs and strengthen their immunosuppressive function. CAFs promote NETosis and M2 polarization of TMAs in the TME by releasing amyloid β or IL8. However, TGF-β secreted by CAFs suppresses Th cell function and reduces CTL infiltration. The expression of PD-L2 and FasL induces AICD in CTLs. CAFs can suppress the DC-mediated antitumor T cell response and inactivate NK cell-mediated tumor killing by PGE2 and IDO secretion. TME: tumor microenvironment; Th: T helper cell; Treg: regulatory T cell; MDSC: myeloid-derived suppressor cell; TAM: tumor-associated macrophage; NK cell: natural killer cell; AICD: activation-induced cell death