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. 2023 Aug 23;8:312. doi: 10.1038/s41392-023-01545-x

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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. 2 — A20 inhibited anti-tumor immune response in vitro. a The flow cytometry analysis of HLA-A2. b The lymphocytoxicity effect of PBMCs on THC8307 cells when A20 expression was manipulated by overexpression (OE) or short hairpin silencing (sh). c The ELISA analysis of T cell activation-related cytokines from the co-culture medium of THC8307 cells and PBMCs, n = 3. d, e The effect of A20 expression on lymphocytoxicity and cytokine release from the co-culture medium of CaCO2 cells and PBMCs, n = 3. f–i The effect of PD-1 inhibitor on lymphocytoxicity and cytokine release from the co-culture medium of A20-knockdown CRC cells and PBMCs, n = 3. All experiments were performed in triplicate. Data was represented as the mean ± SD. *p < 0.05; **p < 0.01; ***p < 0.001; n.s not significant