CD8⁺ T cell priming relies on the ability of dendritic cells (DC) to present antigen as well as recognising, processing and communicating contextual cues associated with antigen acquisition to CD8⁺ T cells. DC often require CD40-CD40L-mediated interactions with helper CD4⁺ T cells to generate an efficient CD8⁺ T cell response. Precisely how such ‘T cell help’ is delivered in vivo and how it optimizes the priming capacity of DC remains unclear. Previous work conducted by the team showed that CD8⁺ T cell priming following HSV-1 skin infection depends on DC receiving both, innate stimulation via IFN-α/β and a help signal from CD4⁺ T cells to provide IL-15 required for effective CD8⁺ T cell priming. Extending the conclusion that T cell help amplifies the innate pathways induced in IFN-α/β-stimulated DC, this study was designed to explore the molecular mechanisms underpinning such help phenotype. Focusing on IL-15, IL-6 and IL-12p40, we have observed differential patterns and dynamics of CD40-induced amplification following IFN-α stimulation. This capacity to flexibly regulate varying cytokine pathways was related to the ability of CD40 to interact with various members of the TNF receptor-associated factor (TRAF) family. The involvement of TRAF6 determined if CD40 stimulation amplifies IL-15, IL-6 or IL-12p40 responses within stimulated DC. These findings argue for a complex regulatory network underpinning T cell help, in which innate signals selectively activate or inhibit distinct arms of the CD40 signalling cascade. By dissecting how T cell help amplifies innate signals required for CD8⁺ T cell priming, this work will assist in the development of more targeted T-cell-based therapeutic strategies.