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. 2020 Mar 20;11:1494. doi: 10.1038/s41467-020-15188-x

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© The Author(s) 2020

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. 10 — a, b Kaplan–Meier analyses of breast cancer patients, associating CXCR3⁺ cell signature (CXCR3S) with distant metastasis-free (DMF) survival (a, TOP trial data set, n = 107 patients) or overall survival (b, compiled data set from basal-like breast cancers, KM plotter, n = 153). Median cutoff was used to group samples into CXCR3S low and high. HR hazard ratio. P values were determined by log-rank test. c Model summarizing interactions between metastasis-initiating breast cancer cells and fibroblasts in the lungs. High JNK activity induces IL-1α/β production in metastasis-initiating cells that furthers JNK signaling in an autocrine fashion. The positive feedback loop increases IL-1α/β levels secreted by cancer cells. Fibroblasts respond to IL-1α/β via type I IL-1R signaling and NF-κB-mediated upregulation of CXCL9/10 that promote metastatic colonization via CXCR3 expressed by metastasis-initiating cells.