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. 2021 Sep 10;40:285. doi: 10.1186/s13046-021-02053-y

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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. 3 — CD112/CD155 and CD226/TIGIT/CD112R/CD96 pathway: CD226, TIGIT, CD112R, and CD96 on T and NK cells bound with their ligands CD112 and CD155 on tumor cells with different affinity. Upon binding, residues in cytoplasmic tails of CD226, CD112R, TIGIT, and CD96 were phosphorylated and produced co-stimulatory or co-inhibitory signals. (reviewed elsewhere [55])