Adoptive cell therapies can produce potent anti-tumor responses in melanoma, yet resistance often emerges within an immunosuppressive tumor microenvironments. Indoleamine 2,3-dioxygenase 1 (IDO1) catabolizes tryptophan to kynurenine, thereby generating immunosuppressive metabolites that inhibit effector T cell function. Using B16 melanoma cells engineered to overexpress IDO1 (B16IDO1), we show that tumor-derived IDO1 promotes resistance to cellular immunotherapy by impairing T cell trafficking, infiltration, and cytotoxicity. B16IDO1 tumors exhibited elevated kynurenine, reduced CXCL9/10 and CCL5, and decreased infiltration of Pmel CD8 T cells, Trp1-specific CD4 T cells, and TRP1-targeted CAR T cells. In vitro, conditioned media from IDO1-expressing tumor cells reduced T cell-mediated killing, and this effect was reversed by IDO1 inhibition. In vivo, adoptive transfer of PMEL or TRP1-specific T cells failed to control B16IDO1 tumors, correlating with reduced intratumoral T cell abundance and effector function. Complementary analyses of patient TIL, tumor, and serum samples are underway to assess correlations between IDO1/Kyn levels and immune cell burden. Ongoing studies extend these findings to human settings, including IDO1+ melanoma xenografts and CAR T cells, to explore the translational potential of targeting the IDO1-Kyn-AHR axis to enhance the efficacy of cellular immunotherapy. These findings highlight a previously underappreciated role for tumor-intrinsic IDO1-mediated immunosuppression that has largely been overlooked in the context of adoptive T cell therapies.