Fig. 2

TLR-MyD88 signaling triggered by TBI is critical for augmenting the antitumor activity of transferred CD8⁺ T cells. Tumor bearing mice were given tripartite ACT therapy consisting of an infusion of 1e⁶ transgenic pmel-1 CD8⁺ T cells with a TCR that recognizes the gp100 peptide on B16 tumors, a viral vaccination encoding gp100 peptide and IL-2 cytokine support in WT versus MyD88 deficient animals with or without 5Gy TBI. a The effectiveness of treatment was decreased in irradiated mice genetically deficient in MyD88. WT and MyD88^–/– tumor-bearing mice were irradiated and then received ACT treatment or were left untreated. Data (mean ± SEM; 5 mice per group) are representative of 2 independent experiments. 5Gy PFI > WT vs. 5Gy PFI > MyD88^-/-, **P < .01, ANOVA. b TBI compromises the colon. Colon of mice were analyzed at 3 days post-TBI and scored by a pathologist unaware of the treatment groups. Data shown (3 mice per group) are representative of 5 independent experiments. *P < .05, unpaired t test. c TBI promotes translocation of gut-derived LPS. Serum from non-irradiated and 5Gy irradiated mice were collected and analyzed for the presence of LPS using a LAL assay 6 days after TBI. Data shown (3 mice per group) are representative of 5 independent experiments. *P < .05, unpaired t-test