Fig. 4
Wnt1 overexpressing tumors depend on DC signaling to evade T cells. Intratumoral cDCs were analyzed by FACS. a Percentages of b-catenin active cDCs, MFI of b-catenin in cDCs, absolute number of b-catenin active cDCs and representative histogram plots (Left). Percentages of b-catenin active CD8+ T cells (right). b Histograms showing b-galactosidase expression (%) by intratumoral cDCs of Axin2LacZ Wnt-reporter mice (Left) MFIs and absolute numbers of galactosidase expressing cells (right). c FACS plots depicting the depletion efficiency of intratumoral cDCs in zDC mice after DT injection (Left). Tumor burden (total absolute number of LLC cells) in sham vs. DT-treated (cDC-depleted) zDC mice (right). d Naive OTI T cells were co-cultured with purified cDCs from Wnt1-overexpressing vs. control OVA-LLC tumors. TCR pathway activation (p-S6 and p-AKT) and cytotoxic molecule expression (granzyme B) were measured by FACS. e OTI T cells that had been primed by intratumoral cDCs as in d were adoptively transferred to mice bearing established subcutaneous OVA-LLC tumors. Graph depicts tumor growth. f Healthy mice were co-adoptively transferred with naive OTI T cells and purified cDCs from Wnt1-overexpressing vs. control OVA-LLC tumors. After 5 days mice were transplanted with OVA-LLC tumors. Graph depicts tumor growth. a–f Cell numbers and profiles were assessed by FACS. Error bars represent mean with SEM. Data are representative or cumulative of at least two independent experiments with 4–9 mice per group. *p < 0.05; **p < 0.01, Mann–Whitney. Source data are provided as a Source Data file
