Cytokine- and checkpoint inhibitor-based immunotherapy for melanoma has resulted in instances of complete and durable remission. However, response to therapy is still less than 60% and is often accompanied by severe adverse reactions and high systemic toxicity. An alternative approach utilises the transfer of large numbers of tumour-specific T cells, often given in combination with total body irradiation. However, due to concomitant damage to precursor cells within the bone marrow, total body irradiation often requires additional bone marrow transplantation for survival. In my project, I aim to determine whether anti-melanoma responses can be generated in mice in the absence of total body irradiation through the pre-programming of T cells before transfer. Tc17 cells are CD8+ T cell subsets that have been reprogrammed ex vivo to secrete interleukin-17. Unlike Tc1 cells (where CD8+ T cells have been programmed to secrete large amounts of interferon-gamma), the mechanisms of Tc17 killing are not fully understood. We plan to adoptively transfer tumour specific Tc17 and Tc1 cells from TRP-2 transgenic mice into sub-lethally irradiated C57BL/6J mice bearing a range of melanoma subtypes. TRP-2 is a self-antigen expressed on melanocytes and melanoma which has not been studied as a target for the reprogramming of tumour specific CD8+ T cells. We plan to utilise bacterial lipopolysaccharide to stimulate the innate immune system to support Tc17 and Tc1 survival and function in vivo. To date, we have demonstrated the capacity of TRP2 CD8+ T cells to kill 3 melanoma lines (B16F10, YUMM 1.7, and YUMM 3.3) in vitro, and we have established the conditions needed to reprogram TRP2 CD8+ T cells to become Tc17 or Tc1 cells. We hope our work will further our understanding of how the immune system can be targeted for therapeutic benefit and in particular, the induction of durable melanoma regression.