Fig. 4.

IFN-γ is a critical contributor to the mechanism underpinning ATI with TLR agonists. The importance of IFN-γ during ATI was assessed using IFN-γ and IFN-γR knockout mouse strains and antibody-mediated cytokine depletion, according to the schedule described in “Materials and methods”. Survival times for B16F10-bearing wild-type mice were also assessed, with graphs representing three independent experiments (n = 8–10, P values were calculated using the Log-Rank (Mantel–Cox) test). a Complete abrogation of IFN-γ was achieved by delivering 250 μg of the H22 antibody clone i.p. twice weekly for the duration of the experiment. The resulting Kaplan–Meier survival curve demonstrated that IFN-γ was critical during ATI with TLR agonists. b Treatment of IFN-γ knockout mice with IFN-γ-competent pMel T cells and TLR agonists further demonstrated that IFN-γ produced by pMel T cells was sufficient for the needs of the therapy. c Successful treatment of IFN-γR knockout mice via ATI with TLR agonists demonstrated that host responses to IFN-γ were not necessary for therapy