Dendritic cells (DC) are pivotal for initiating adaptive immunity, a process triggered by the activation of DC via pathogen products or damage. Here, we describe an additional layer to this process, essential when pathogen-derived signals alone cannot directly achieve full DC activation. Immunisation with sporozoites from Plasmodium leads to CD8 T cell priming in a complex response that is initiated by a collaboration between conventional type 1 DC (cDC1) and γδ T cells, underpinned by production of IL-4. We have shown that IL-4 has three key functions in this response: 1) it acts directly on cDC1 to enhance production of IL-12, 2) it acts directly on CD8 T cells to enhance their expansion and 3) it induces differentiation of the expanding CD8 T cells to form liver resident memory T (TRM) cells. The IL-4 induced liver TRM cell differentiation is dependent on IL-4 receptor signalling via the transcription factor STAT6, which induces a liver TRM cell transcriptional program. Importantly, the IL-4 program leads to higher numbers of liver TRM cells, which provide enhanced protection against parasites upon challenge infection. These insights demonstrate that responses to some pathogens require help from innate-like T cells to pass a DC activation threshold to initiate and further amplify the response and underscore the potential of IL-4-directed vaccination strategies to enhance liver TRM -mediated protection against liver-tropic pathogens and malignancies.