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. 2022 Aug 30;20:384. doi: 10.1186/s12967-022-03574-6

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© The Author(s) 2022

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. 8 — SPOP can promote the immune tolerance of PD-1 via CXCL16. A CXCL16 transient siRNA-knockdown in HeLa cells with SPOP knockdown did not increase SPOP expression, but only reduced the increased-CXCL16 expression. B–D The results of CCK-8, colony formation and invasion assays showed that CXCL16 knockdown could reverse these phenotypes. E, F The IC50 results showed that CXCL16 knockdown could functionally reverse immune tolerance