Current immunotherapies directed at enhancing the quality of CD8⁺ T cell responses show remarkable promise, but their efficacy in patients with solid tumours is limited. This is mediated in part by tumour-specific T cells being inefficiently recruited or actively excluded from the tumour parenchyma. Thus, understanding the chemotactic cues that dictate T cell trafficking into tumours is critical in finding strategies to enhance clinical responses. The atypical chemokine receptor 4 (ACKR4) is widely expressed among tissues and acts to regulate the availability of the T cell-attracting chemokines CCL19, CCL21 and CCL25. Here, we have identified a novel role for ACKR4 in repressing anti-tumour immunity, using the E0771 and transgenic MMTV-PyMT models of breast cancer. ACKR4 expression in the tumour microenvironment is upregulated over the course of tumour progression. In the absence of ACKR4, increased levels of intratumoural CCL21 are associated with enhanced recruitment of IFNg⁺ CD8⁺ T cells to mammary tumours, with unaffected recruitment of Foxp3⁺ and Foxp3^- CD4⁺ T cells. This leads to a significant inhibition in tumour growth, with depletion of CD8⁺ T cells restoring growth to wildtype levels. Furthermore, inhibition of tumour growth by deletion of ACKR4 is also seen in orthotopic and chemically-induced models of skin cancer. These data support the notion that ACKR4 is a critical regulator of the tumour microenvironment by preventing recruitment of anti-tumour T cells through scavenging of CCL21.