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. 2023 Jul 26;14(7):466. doi: 10.1038/s41419-023-05961-3

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© The Author(s) 2023

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — TIGIT, CD226, CD96, and CD112R are expressed in T cells and NK cells. The ligands CD155 and CD112 are expressed on tumor cells or APCs. TIGIT delivers inhibitory signals by binding to CD155 and CD112, with the highest affinity for CD155. CD226 and CD96 compete with TIGIT for binding to CD155, but with lower affinity than TIGIT. CD226 delivers activating signals. However, whether CD96 triggers inhibitory or activating signals remains to be determined. CD112R and CD226 also competitively bind to CD112, with higher affinity with CD112R. APCs, antigen-presenting cells.