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 tumors and immune escape of antigen negative variants. 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 therapy, and that DC activation is associated with enhanced responses to CAR T cell therapy. We hypothesised that engaging the endogenous immune system through enhancing host DCs will improve T cell responses and overcome the challenges of tumor 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 an increased recruitment of host T cells to the tumur and draining lymph nodes (dLN). Strikingly, combination of FL-secreting T cells with adjuvants resulted in inhibition of tumor growth and improved survival in two mouse models of ACT for breast and colorectal tumors. This was associated with an increased number of activated DCs and functional host T cells in the dLN following combination therapy, suggesting that this therapy is capable of inducing epitope spreading and eliminating tumors that are negative for the antigen 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 tumor escape following therapy.