Fig 2: Construct of the immune-related gene prognostic index (IRGPI) in TNBC. (a) Kaplan–Meier survival analysis of AIM2, CCL5, and CCL25 genes that are significant in the univariate Cox analysis (p < 0.05); (b) univariate and multivariate Cox regression analysis of survival-related genes; (c) Kaplan–Meier survival analysis of IRGPI scores using TCGA data and the relationship between the survival status and IRGPI score distribution in the TCGA TNBC cohort; (d) ROC curves of the prognostic models in TNBC (the TCGA cohort) at 1, 3, 5, and 7 years; (e) expression of CCL25, CCL5, PD-L1 in TNBC. (a) Representative samples with CCL25 positive (above) and negative (below) expression; (b) representative samples with CCL5 positive (above) and negative (below) expression; (c) representative samples with PD-L1 positive (above) and negative (below) expression. Scale bars: 200 µm for the left pictures in (a–c), and 50 µm for the right pictures in (a–c); (f) Kaplan–Meier survival analysis of CCL5 and CCL25 expression and IRGPI groups using IHC scores of the patients from our hospital (p < 0.05).

Fig 3: Proposed model of TECK-induced migration and invasion, and inhibition of apoptosis in human breast cancer cells. TECK, thymus-expressed chemokine.

Fig 4: IRGPI is associated with T-cell exclusion and dysfunction, and PD1 and PD-L1 expression in TNBC of TCGA data set. (a) Scores of TIDE, MSI, and T-cell exclusion and dysfunction in different IRGPI risk groups (ns: not significant, ** p < 0.01; *** p < 0.001); (b) Correlation between CCL5/CCL25/ IRGPI scores and PD-L1/PD1.

Fig 5: Recombinant protein CCL25 increased endothelial permeability and CCL25 expression in HPMECs. HPMEC were treated with 0, 25, 50, 100 and 200 ng/mL recombinant CCL25. (A) TEER assay. (B) FITC fluorescence intensity assay. P<0.05 indicated significant difference, *P<0.05, **P<0.01, ***P<0.001. The experiments were repeated three times.