Fig 2: Kaplan-Meier analysis of OS according to IDO expression. Differences between curves were assessed by the log-rank test. A: patients in the entire cohort (n=183). B: patients with stage I disease (n=52). C: patients with stage II disease (n=41). D: patients with stage III disease (n=71). E: patients with stage IV disease (n=19). F: patients treated without radical resection (n=27). G: patients treated with radical resection (n=156).

Fig 3: Before and after oxLDL treatment, the IFN-γ-mediated promotion of THP-M foaming was reversed by IDO1 inhibition. a, b IDO1 activity (Kyn/Trp) was detected by HPLC. c, d The results of Oil red O staining (×400). The designation of different treatments, such as oxLDL, IFN-γ, IFN-γ+oxLDL, oxLDL+IFN-γ, IFN-γ+Incyte+oxLDL, oxLDL+IFN-γ+Incyte, IFN-γ+1-MT+oxLDL and oxLDL+IFN-γ+1-MT, was described in the Materials and Methods. Data were based on at least three independent experiments. *p < 0.05

Fig 4: Features of keratinocytes overexpressing IDO. a. Quantitative reverse transcription polymerase chain reaction was used to detect the gene expression of IDO. (∗∗∗P < 0.001, n = 3). b. Expression of IDO protein was evaluated in the Control, NC and IDO group by Western blot analysis (∗∗∗P < 0.001, n = 3). c. Kynurenine levels in IDO transfected keratinocytes conditioned medium. Conditioned medium was collected from the same number of infected and non-infected cells at 72 h post-transfection. Kynurenine levels were determined (∗∗∗P < 0.001, n = 3). d. CCK8 assay showed the proliferative ability of Control, NC and IDO group (n = 3). e. Transwell test was used to analyze cell migration, and the number of positive cells was counted. (Scale bar, 10 μm n = 3). f. Analysis of apoptosis of CD8+ T lymphocytes by flow cytometry (∗∗∗P < 0.001, n = 3).

Fig 5: Evaluation of US-associated IDO1 genome editing in vitro.a Representative CLSM images of 4T1 cells with different treatments from three biologically independent samples. Concentration = 100 μg/mL. Incubation time = 12 h. b Illustration of transfection process of 4T1 cells by MHS upon US. c Toxicity evaluation in 4T1 after incubated with different concentrations of MHS and (d) Cell viability of 4T1 cells after various treatments for 24 h (n = 5 biologically independent samples). e Flow cytometry analysis of apoptosis of 4T1 cells with various treatments (n = 3 biologically independent samples). f Representative CLSM images and g corresponding mean fluorescence intensity of 4T1 cells treated with various treatments after IFNγ-stimulation, followed by staining with fluorescent anti-IDO antibody (red). DAPI was used to stain the nucleus of the cell (blue) (n = 3 biologically independent samples) h In vitro DNA sequencing of IDO1 in 4T1 cells after treatment with MHS and MHS + US. i Representative image of T7EI cleavage analysis after 4T1 cells with different treatments. j Deep sequencing analysis of gene editing in 4T1 cells in the presence of MHS and (k) MHS + US. The experiments for h, i, j, and k were repeated three times independently with similar results. Statistical differences for c, d, and g were calculated using two-tailed unpaired Student’s t-test for comparisons between two groups, ordinary one-way ANOVA for comparisons of more than two groups not containing Control, and Dunnett’s multiple comparisons post test for comparisons of more than two groups containing Control. Data were expressed as means ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Source data are provided as a Source Data file.