Adoptive cell therapy (ACT) using chimeric antigen receptor (CAR) T cells is a form of immunotherapy that involves the genetic engineering and re-infusion of a patient’s own T cells to specifically target cancer. While CAR T cells have had a significant impact in some haematological malignancies, its efficacy in solid cancers have been limited to date. A major factor limiting its success is the heterogeneity of tumours and immune escape of antigen negative variants1. Dendritic cells (DCs) are professional antigen presenting cells specialised in the priming and activation of T cells, leading to their expansion and increased effector function. We previously show that DCs play a crucial role in immune checkpoint blockade therapy2, and that DC activation is associated with enhanced responses to CAR T cell therapy3. We hypothesised that engaging the endogenous immune system through enhancing host DCs will improve T cell responses and overcome the challenges of tumour heterogeneity in ACT. To this end, we engineered T cells to secrete Fms-like tyrosine kinase 3 ligand (FL), a growth factor critical for the development of DCs. Mice treated with FL-secreting T cells showed expanded DC and precursor populations, and increased recruitment of host T cells to the tumour and draining lymph nodes (dLN). Combination of FL-secreting T cells with adjuvants resulted in inhibition of tumour growth and improved survival in two mice models of ACT for breast and colorectal tumours. Importantly, combination therapy using FL-secreting CAR T cells resulted in epitope spreading, suggesting that this approach is capable of inducing anti-tumour responses beyond antigens targeted by the CAR. Our data suggest that enhancing endogenous DCs is a promising strategy to augment the efficacy of CAR T cells in solid cancers and may help combat the clinical problem of antigen negative tumour escape following therapy.