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. 2024 Feb 21;21(4):374–392. doi: 10.1038/s41423-024-01133-1

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© The Author(s) 2024

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 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/.

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Fig. 8 — Tumor-infiltrating Ki67⁺CXCL13⁺CD4⁺ T cells enriched with the IFN-I signature are associated with better clinical outcomes in cancer patients. Tumor-infiltrating Ki67⁺CXCL13⁺CD4⁺ T cells enriched with the IFN-I signature are associated with better clinical outcomes in cancer patients. A, B Heatmaps depicting the average expression values of signature genes of the A CXCL13⁺ T-helper tumor-specific cell (Tht) signature [40] and the B tumor-infiltrating CD4⁺ T cells in CE9 [19] in the five tumor-infiltrating FOXP3^-CD4⁺ T-cell clusters that we identified. C Kaplan–Meier curves revealing the prognostic value of the tumor-infiltrating CD4⁺ T-cell clusters that we identified for overall patient survival in the BRCA, COAD, LIHC, LUAD, OV, READ and SKCM cohorts from the TCGA database (n = 3156). The high and low metagene expression subgroups of patients were identified based on a threshold of the quartile expression level. D Box plots depicting the enrichment scores of tumor-infiltrating CD4⁺ T-cell clusters in responders (R) and nonresponders (NR) to anti-PD-1 immunotherapy [42]. E–K ScRNAseq data of tumor-infiltrating FOXP3⁻CD4⁺ T cells from HPV⁺ OPSCC patients (n = 43) were analyzed. The patients were stratified into the immune response-positive (IR⁺, n = 6) and immune response-negative (IR⁻, n = 4) groups based on the presence or absence, respectively, of tumor-specific T-cell infiltration. E, F UMAP plot and compositions of the eight clusters identified in the IR⁺ and IR⁻ groups. Heatmaps depicting the average expression values of G the tumor-infiltrating CD4⁺_MKI67 signature that we identified, H the CXCL13⁺ Tht signature [40] and (I) the tumor-infiltrating CD4⁺ T-cell signature in CE9 [19] in each cluster. J Percentages of cluster 3 and 4 cells among CD4⁺ T-cells from patients in the IR⁺ and IR⁻ groups. K Heatmaps depicting the expression of the IFN-I signature in tumor-infiltrating CD4⁺ T cells in clusters 3 and 4. L Schematic illustration depicting the mechanism of cDC1 licensing mediated by IFN-I-producing CXCL13⁺CD4⁺ T cells in the proinflammatory TME (CE9) [19]. P < 0.05*, P < 0.01** (log-rank test/Mantel–Cox test in C; Mann–Whitney U-test for J). The data are shown as the means ± SEM