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. 2021 Oct 16;40:327. doi: 10.1186/s13046-021-02128-w

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© The Author(s) 2021

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 — Microbial stimulation of inhibitory checkpoints modulates the tumor immune microenvironment. Fusobacterium nucleatum inhibits the activity of natural killer cells and cytotoxic T cells via interaction between Fap2 and TIGIT or CEACAM1. Helicobacter pylori acts on CEACAM1 through its outer membrane protein HopQ protein to inhibit immune cells. Bifidobacterium upregulates the expression of IFN-I in dendritic cells through the STING signaling pathway, thereby promoting antigen cross-presentation and T cell activation to enhance the efficacy of CD47 blockade. Abbreviations: STING = the stimulator of interferon gene