Th17-polarized TRP-1 CD4+ T cells reject tumor in an IFN-γ–dependent mechanism. (A) In vivo neutralization of cytokines after adoptive transfer of Th17 TRP-1 cells. Sublethally irradiated (500 R) tumor-bearing C57BL/6 mice were treated with 1 × 106 Th17 TRP-1 cells and injected intraperitoneally every other day with 100 μg neutralizing antibodies directed against IFN-γ, IL-17A, IL-23, or isotype control antibody. Results for tumor area are the mean of measurements from at least 5 mice per group (± SEM). Data shown are representative of 3 independent experiments (NT vs Th17, P = .003; NT vs Th17 anti–IFN-γ, P = .558; Th17 isotype vs Th17 anti–IL-17A, P = .117; Th17 isotype vs Th17 anti–IL-23, P = .754). (B) Tumor-bearing C57BL/6, (C) IFN-γ−/−, and (D) IFN-γ receptor–deficient (IFN-γR−/−) mice were treated with 1 × 106 Th1- and Th17-polarized TRP-1 CD4+ T cells. Tumor growth was measured as described previously (± SEM, n = 5-8; NT vs Th17, P < .001 in C57/BL6 hosts, P < .05 in IFN-γ−/− hosts, and P < .05 in IFN-γR−/− hosts).
