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. 2022 Mar 21;126(10):1470–1480. doi: 10.1038/s41416-022-01763-0

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© The Author(s) 2022

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 — a Experimental setup used in (b–f): C57BL/6 mice were intraperitoneally injected with 1 × 10⁷ ID8-Trp53^−/−Control (Ctrl) or ID8-Trp53^−/−Cxcl9⁺ (Cxcl9⁺) cells and treated with 200 µg anti-PD-L1 antibody or corresponding IgG2b isotype control. b, c Soluble Cxcl9 or Cxcl10 in murine ascites of groups listed under section (d) was quantified by ELISA and normalised to total protein. d Kaplan–Meier plots with time to ascites formation (left) and overall survival (right) of anti-PD-L1 or IgG2b-treated groups stratified by Cxcl9 overexpression in the ID8-Trp53^−/− model (n = 7 in each group). e, f Digital analysis of immunohistochemically detected immune cell population markers (CD3, CD8, Foxp3) and Ki-67-positive tumour cells within the tumour microenvironment. Each dot indicates the data of one individual mouse. Bars represent mean ± SEM.