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Fig. 5 | Molecular Cancer

Fig. 5

From: Acidosis-mediated increase in IFN-γ-induced PD-L1 expression on cancer cells as an immune escape mechanism in solid tumors

Fig. 5

Tumor growth upon a combinatory or mono-treatment with NaHCO3 and anti-PD-L1 in anti-PD-L1 responsive and nonresponsive tumor models. A Tumor volumes of MC38wt (n = 8 animals per group), B MC38PD−L1−/− (n = 4–5 animals per group), C IFN-γ knockout mice (neutral and acidosis, n = 7–8 animals per group). D CT26wt (n = 7–8 animals per group), and E CT26PD−L1−/− (n = 8 animals per group) tumor volumes  of mice treated with NaHCO3 and/or anti-PD-L1 mAb. F Tumor volumes of B16-F10wt (n = 5–8 animals per group) and (G) 4T1wt tumors (n = 5–8 animals per group) growing in mice treated with NaHCO3 and/or anti-PD-L1 mAb. Treatment with NaHCO3-enriched water (200 mM, NaHCO3) started three days prior to cancer cell inoculation; anti-PD-L1 mAb (200 µg per mouse) was administered every third day starting on day 4 (MC38wt, CT26wt, B16-F10wt) or day 5 (4T1wt) after the cancer cell inoculation. Tumors from mice with intact IFN-γ signaling that received regular drinking water developed an acidic tumor pHe (Control). Data are presented as the means ± SEM. Statistics: Tukey’s multiple comparison test (A, C, D, and F) and Sidak’s multiple comparison test (B and E)

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