Correction: CXCL10-induced regulatory T cells and adenosine signaling promote immunosuppression and progression of epithelial ovarian cancer

Correction to: Scientific Reports https://doi.org/10.1038/s41598-025-06812-1, published online 01 July 2025

The original version of this Article contained errors in the order of the figures. Figure 2 was published as Figure 3, Figure 3 was published as Figure 2, Figure 6 was published as Figure 7, and Figure 7 was published as Figure 6. The Figure legends were correct at the time of publication.

The original Figures 2, 3, 6 and 7 and accompanying legends appear below.

Figure 2

Cytokine profiling of conditioned media from PEO1 and PEO4 cells. PEO1 and PEO4 cells were treated with IFNγ, stattic, or both in combination for 24 h. Conditioned media were collected to determine the levels of 36 cytokines using a cytokine immunoarray. The levels of representative cytokines produced by PEO1 and PEO4 cells are shown (A). Conditioned media of PEO1 and PEO4 cells under normal growth conditions after 24 h were collected to determine the levels of 105 cytokines using a cytokine immunoarray. The levels of cytokines over-produced by PEO1 cells (B) or by PEO4 cells (C) were shown. PEO1 and PEO4 cells produced comparable levels of MIF, which are also demonstrated. Data are means ± SD (n = 2) of duplicate measurements from a representative experiment.

Figure 3

Immunosuppressive effects of PEO1 and PEO4 cells on PBMCs and SUPT1 cells. PBMCs or SUPT1 cells activated by CD3/CD28 antibodies were co-cultured with PEO1 or PEO4 cells for 48 h. PBMCs were collected, stained, and analyzed by a flow cytometer to determine the percentage of the CD8 + CD25 + T cell population in PBMCs (A) and in SUPT1 cells (B), as well as the percentage of the CD4 + CD25 + T cell population in PBMCs (C). To determine the level of the Treg population, PBMCs were first gated for CD4 + cells to determine the percentage of the CD4 + T cell population in PBMCs (Top). The CD4 + T cell population was subsequently gated for FXOP3 + CD25 + cells to determine the percentage of FOXP3 + CD25 + T cells in the CD4 + T cell population (bottom). The bar graph shows the percentage of FOXP3 + CD4 + CD25 + T cells in PBMCs by calculating FOXP3 + CD25 + T cells of CD4 + T cells of total PBMCs (D). Data are means ± SD (n = 3) from three independent experiments.

Figure 6

CXCR3 and CCR5 expression in T cell subsets in human PBMCs. Levels of CXCR3 and CCR5 RNA expression (nTPM) in MAIT T cells, CD8 T cells, Tregs, and PBMCs were shown, using the Monaco (n = 4–13) (A) and HPA (n = 5–6) (B) datasets from the Human Protein Atlas. MAIT, mucosal-associated invariant T cells. Heatmap of RNA expression levels of T cell markers, CXCR3, and CCR5 in various immune cell types. The color indicates the level of scaled mean RNA expression. The heat map was generated from the dataset of the Single Cell Portal. CD3E is used as a T cell marker to highlight CD8 + cytotoxic T cells and CD4 + (or FOXP3 +) T cells (C).

Figure 7

Efficacy of CXCR3 blockade on peritoneal progression of p53(-/-) ID8 EOC and the survival of C57BL6 mice. Mice (Control group, n = 5; CXCR3 mAb group, n = 4) were inoculated ip with ID8 cells and treated ip with vehicle or CXCR3 mAb for 5 weeks. The ACs of mice were measured to determine the percentage increase in AC. The body weight of mice was measured to monitor treatment toxicity (A). The Kaplan–Meier survival curve and median survival time of mice were determined using a 50% increase in AC as the endpoint (B). Mice (n = 5) were inoculated ip with ID8 cells and treated ip with vehicle, AMG487, bevacizumab (Bev), or both in combination for 5 weeks. Bev group, n = 4. The ACs of mice were measured to determine the percentage increase in AC. The body weight of mice was measured to monitor treatment toxicities. Data are means ± SD.*, p < 0.05; **, p < 0.01 (C). The Kaplan–Meier survival curve and median survival time of mice were determined using a 50% increase in AC as the endpoint. p values are shown (D). Mice (n = 5 and n = 3 from two experiments) inoculated ip with ID8 cells were treated with vehicle or AMG487 for 5 weeks. When mice reached the survival endpoint, tumor ascites was obtained and CD3 + T cells were isolated, stained, and analyzed by a flow cytometer to determine the percentages of activated CD8 + T cells and FOXP3 + CD4 + Tregs in total CD3 + T cells. Each dot represents the value of an individual mouse. Means and SD of all mice in each treatment group, and p values are shown (E).

The original Article has been corrected.