Treatment options for triple negative breast cancer (TNBC) are currently limited to chemotherapy, resection of tumour mass and radiotherapy. Responses to these treatment options are often underwhelming, resulting in rapid spread of metastasis which attributes to the majority of deaths within the first 24 months. This highlights the urgent need for novel treatment options that stimulate a long-lived memory immune response. One problem facing the development of new therapeutics is the ‘invisibility’ of these tumour cells to the immune system that occurs from a downregulation of the MHC-I antigen presentation pathway. Furthermore, past studies have demonstrated that TNBCs have decreased tumour-inherent interferon production, which is known to drive MHC-I expression. Here, we demonstrate that re-induction of the IFN-pathway within murine TNBC cell lines leads to enhanced recognition of tumour cells by CD8+ T cells. We overcome the previously demonstrated widespread toxicity from systemic administration of IFN through delivery of an IFN-inducer directly into the primary tumour in a murine neoadjuvant treatment regime. This therapy was able to alter tumor visibility, demonstrated by dramatic increases in the number of intratumoural-specific CD8 T cells. Moreover, we observed a decrease in immune suppressive populations, myeloid derived suppressor cells (MDSCs) and regulatory T cells (Tregs), within primary tumours. Overall this lead to decreases in primary tumour size, metastasis to the lung and bone and ultimately increased survival in both resection and non-resection regimes of the highly aggressive 4T1.2 murine TNBC model. Furthermore, intratumoural IFN-induction further enhanced survival to chemotherapy when combined in a clinically relevant neoadjuvant treatment setting. We believe intratumoral delivery of this IFN-inducer is a viable neoadjuvant treatment option for human TNBC which may bolster chemotherapeutic responses and ultimately prevent metastatic spread.