Adoptive cell transfer (ACT) therapy using patient-derived T cells genetically engineered to express a chimeric antigen receptor (CAR) is highly effective in B cell malignancies and is now FDA-approved. However, tumor heterogeneity remains a major challenge in treating solid tumors due to the relapse of tumors negative for CAR-targeted antigen. Previously we demonstrated that CAR T cells engineered to secrete dendritic cell (DC) growth factor Fms-like tyrosine kinase 3 ligand (Flt3L) promote host anti-tumor immunity to effectively eradicate heterogenous tumors by expanding intratumoral conventional type 1 dendritic cells (cDC1) (Lai et al. 2020 Nat Immunol). cDC1 is well-reported to be a critical mediator in activation of anti-tumor cytotoxic responses. A key aspect of this study was that despite the increased population of intratumoral cDC1s, cDC1s required a second activatory stimulus to elicit anti-tumor immunity. Here, we explored the possibility of leveraging the CD40 axis to promote cDC1 function and synergise with Flt3L-secreting ACT therapy. Engagement of upregulated CD40 on antigen-experienced DC with its ligand CD40L, which is traditionally expressed on activated T cells, induces DC activation. The effect of activation was observed via the upregulation of co-stimulatory molecules, CD80 and CD86, indicating DC maturation and expansion of tumor-antigen specific T cells upon anti-CD40 activation of Flt3L-expanded cDC1 in vivo. To incorporate the CD40 axis activation in adoptive cell therapy, successful engineering of CAR T cells was conducted using a novel construct to induce high CD40L expression constitutively. Furthermore, as Type I interferon (IFN) potentiates DC activation in response to CD40 stimulation, a CRISPR knock-in strategy developed in our laboratory (Chen et al. 2025 Nature) was employed to induce tumor-localized secretion of IFNβ on CD40L-expressing CAR T cells, enhancing cDC1 activation and differentiation. Improved DC maturation was observed upon adoptive transfer of IFNβ/CD40L-expressing T cells following Flt3L-induced DC expansion, correlated with improved therapeutic efficacy. Based on our results of the synergistic effect between Flt3L and CD40L on cDC1, we are poised to further incorporate this with Flt3L-secreting CAR T cell to achieve cDC1 expansion and activation upon ACT. Our study has demonstrated an enhanced efficacy of CAR T cell treatment in solid cancers by harnessing the endogenous immune responses against tumors.