Fig. 1: R54 impaired Tregs function in primary RCC patients.
From: Targeting CXCR4 impaired T regulatory function through PTEN in renal cancer patients
a Upper panel: CFSE-T effector proliferation in the presence of PB-RCC-Tregs (CD4+CD25+) and PB-HD-Tregs. Tregs were pretreated for 30’ at 37 °C in 5% CO2 with R54 (10 µM) (RCC: 15 ± 3% in 1:1 vs. 50 ± 6% in 1:1 + R54 Teff: Tregs ratio, p < 0.05). The box plot represents the median and spread of data within min to max value (RCC, n = 16; HD, n = 19). Right panel, representative density plots. a Lower panel: IFN-γ, IL-10, and TGF-β1 by ELISA assay in culture supernatant collected on day 5 from CFSE experiments of RCC patients (IFN-γ 1:1 105 ± 7 pg/mL vs. 1:1 + R54 153 ± 12 pg/mL, p < 0.05); IL-10 (1:1 210 ± 18 pg/mL vs. 1:1 + R54 90 ± 8 pg/mL, p < 0.01); TGF-β1 (1:1 11 ± 0.7 ng/mL vs. 1:1 + R54 7 ± 0.2 ng/mL, p < 0.01). The box plot represents the median and spread of data within the min to max value (RCC, n = 5). b PB-isolated Tregs from RCC patients were evaluated by FACS analysis for frequency of CTLA-4, PD-1, and CD40L (CTLA-4+Treg: Tregs 19 ± 1% vs. Treg+R54 9 ± 2%, p < 0.05). Histograms represent the mean ± sem (RCC, n = 3). c Nrp1+Tregs from CFSE assay of RCC patients and HDs (RCC: 3 ± 0.8% in 1:1 vs. 0.3 ± 0.1% in 1:1 + R54 Teff: Tregs ratio, p < 0.05). The box plot represents the median and spread of data within min to max value (RCC, n = 7; HD, n = 6). In the right panel, representative density plots were shown. Paired and unpaired Student’s t-test was used. (*p < 0.05; **p < 0.01; ***p < 0.001). Data are derived from at least three independent experiments.
