Supplementary Figure 5: Low-glycolytic B16 tumors are not rejected by Cremfl/flLyz2-Cre mice.
From: Tumor immunoevasion via acidosis-dependent induction of regulatory tumor-associated macrophages
(a,b), Extracellular acidification rate (ECAR) of (a) indicated tumor cell lines and (b) B16 melanoma sub-lines with high glycolytic activity (B16), low glycolytic activity (Low glycolytic B16) and MC38 colon adenocarcinoma cells (n = 8 each group). The Seahorse assay was repeated four times. Each measurement time point ± s.d. is plotted. (c) Growth of ‘‘Low-glycolytic B16’’ in mice with an ICER-deficiency in myeloid cells (Cremfl/flLyz2-Cre, n = 10) and respective litter-mate control mice (Cremfl/fl, n = 10). 2 × 105 low-glycolytic B16 melanoma cells were inoculated s.c. into the left flank. Tumor development was observed for 21 d. **P ≤ 0.01, ***P ≤ 0.001 using a two-tailed, unpaired t test with Welch’s correction.
