Fig. 6

IRF8 is required for anti-tumour effect of Th9 cells. a WT, Irf8 ^f/f Cd4 ^cre and Irf8 ^+/+ Cd4 ^cre mice were subcutaneously (s.c.) injected with B16F10 cells and tumour growth was monitored. Representative data from one of three experiments are shown (mean and s.e.m., 10 mice per group). b WT, Irf8 ^f/f Cd4 ^cre and Irf8 ^+/+ Cd4 ^cre mice were intravenously (i.v.) injected with B16F10 melanoma cells and 12 days later mean numbers of lung tumour foci are shown (mean and s.e.m., 5 mice per group, 3 independent experiments). c Il4 and Il9 mRNA expression analysis in tumour infiltrated lymphocytes (TILs). d, e Tumour-draining lymph nodes (TDLN) from WT, Irf8 ^f/f Cd4 ^cre and Irf8 ^+/+ Cd4 ^cre mice given a subcutaneous injection of B16F10 cells were collected at day 13. Analysis of Il4 and Il9 mRNA expression in TDLN (d). TDLN cells were stimulated for 72 h in plate-bound anti-CD3 and anti-CD28, and IL-4 and IL-9 release was assessed by ELISA (e). f–h WT mice were injected iv with B16F-OVA melanoma cells or together with effector OT-II Th9 (f, g) or OT-II Th9 + IL-1β (h) cells infected with shRNA control (shCT) or against Irf8 (shIRF8). Representative lung from mice untreated or treated with Th9 cells infected with shCT or shIRF8, 13 days after intravenous injection (f). Mean numbers of lung tumour foci are shown (g, h) (mean and s.e.m., 5 mice per group, 3 independent experiments) ns, not significant; *P < 0.05, **P < 0.01; ***P < 0.001 (Kruskal–Wallis test (b–e, g, h))