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. 2017 Dec 12;8:2050. doi: 10.1038/s41467-017-02281-x

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© The Author(s) 2017

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. 3 — CX3CR1 expression is decreased in Mo-MDSCs in p16/p21-DKO mice. a Identification of the factor regulating p16/p21-dependent Mo-MDSC accumulation using RNA-sequencing data analysis; the Venn diagram shows the numbers of genes overexpressed in Mo-MDSCs compared with those in PMN-MDSCs (fold change >2, p < 0.05) and downregulated in DKO Mo-MDSCs compared with WT Mo-MDSCs (fold change <0.75, p < 0.05) categorised under chemokine receptor activity (biogroup). b Cx3cr1 mRNA expression in PMN- and Mo-MDSCs from WT or p16/p21-DKO mice (n = 3), as determined by qRT-PCR. c Representative flow cytometry histograms showing CX3CR1 expression in PMN- and Mo-MDSCs in BM (left), spleen (middle), and tumour (right) from WT and p16/p21-DKO mice 3 weeks after SCT cell injection. d Mean fluorescence intensity (MFI) of CX3CR1 expression in Mo-MDSCs shown in c (n = 5); data are presented as the mean ± SEM. The statistical significance was determined by Student’s t-test; *p < 0.05 and **p < 0.01; NS not significant