Fig. 6

Blocking TGFβ allows DMXAA-induced type I IFN production and tumor regression. a Spont-PyMT mice, treated with an anti-TGFβ (day − 4 and day − 1), received one i.p. injection of DMXAA. Three hours later, tumors were collected and tumor slices were stained with anti-EpCAM (blue) and anti-pIRF3 (red) mAbs. The image is representative of n = 4 anti-TGFβ-treated Spont-PyMT mice from three independent experiments. Scale bar = 50 µm. b Tumors from Spont-PyMT mice, treated with anti-TGFβ (black circles) or notβ (gray circles), and from Trans-PyMT mice (open circles), were analyzed by flow cytometry for the expression of MHCII on TAM and monocytes. The data are from anti-TGFβ-treated Spont-PyMT mice: n = 7; Spont-PyMT mice: n = 6 or 8; Trans-PyMT mice: n = 12 or 21, for TAM or monocytes respectively, collected in seven independent experiments. The results are expressed as mean ± SEM. Tukey’s multiple comparison test. *p < 0.05; **p < 0.01; ***p < 0.001. c Tumors from anti-TGFβ-treated Spont-PyMT mice were pooled for each mouse (8–10 tumors), dissociated and F4/80⁺ cells were sorted with magnetic beads. F4/80⁺ and F4/80^neg fractions were restimulated in vitro with DMXAA (250 µg/ml, black circles) or not (gray circles) and IFNα was measured by ELISA in the supernatant after overnight culture. The results are expressed as mean ± SEM. Student t test. *p < 0.05; **p < 0.01; ***p < 0.001. d Spont-PyMT mice were treated with DMXAA (i.p. at day 0) or DMSO as a control, with anti-TGFβ (i.p. 200 µg), anti-IFNαR (i.p. 200 µg) and/or with anti-CD8 (i.p. 200 µg) Abs on day − 4, day − 1, day 1, day 4. The proportion of mice with an average regressing, stabilized or progressing tumors, is shown as in Fig. 1. DMSO-treated mice: n = 28; DMXAA-treated mice: n = 30; DMSO + anti-TGFβ: n = 6; DMXAA + anti-TGFβ: n = 9; DMXAA + anti-TGFβ + anti-IFNαR: n = 6; DMXAA + anti-TGFβ + anti-CD8: n = 5. Statistics are shown in Supplementary Table 2. Source data are provided as a Source Data file