Tumour-derived antigens play an important role in both spontaneous and therapeutic anti-tumour immunity. Recent data has revealed how a large majority of tumour-neo-antigens contain MHCII epitopes that can be recognised by CD4+ T cells. However the subsets responsible for presentation of antigen to T cells and the mechanism by which T cells amount anti-tumour responses is not well understood. We have recently demonstrated that tumour-specific CD4+ T cells eradicate established tumours in the absence of direct MHCII recognition and interaction with tumour cells, supporting a role for effective CD4+ T cell immunity against MHCII-negative tumours. Those populations responsible for interactions with CD4+ T cells and presentation of tumour antigens were unknown. We therefore developed a robust 12-parameter flow cytometric gating strategy for simultaneous identification, characterisation and purification of up to 10 tumour infiltrating myeloid subsets. We used both hierarchical clustering of heatmaps and t-SNE clustering analysis for verification of populations and functional analysis. We identified 3 previously unappreciated tumour-infiltrating DC populations that present tumour antigen to CD4+ T cells ex vivo. Using flow cytometric based analysis of population frequency and functional marker expression, we have shown how CD4+ T cells actively alter these DC subsets, and other immune subsets, during anti-tumour responses. Specifically we observed upregulation of both costimulatory and inhibitory markers on tumour infiltrating populations, recruitment of Neutrophils and TAM and loss of pDCs and Eosinophils from the tumour. Furthermore we determined if these immune phenotypes were representative of cancer patient responses and outcomes through analysis of TGCA datasets.