Resolution of intracellular infections relies heavily on the coordination of three immune cells the dendritic cell (DC), the ‘cytotoxic’ CD8 T cell and the ‘helper’ CD4 T cell. Our understanding of how DCs integrate and process the complex information they have encountered still remains incomplete, which is perhaps best documented by our continuing difficulties in generating efficient T cell-based vaccines. In many cases CD4 T cells are essential for the development and maintenance of CD8 T cell responses by delivering signals termed ‘T cell help’ to the DCs who are presenting the pathogen. We recently published that CD4 T cells are able to amplify the DCs pathogen-programmed response to ensure the generation of a robust CD8 T cell response essential for pathogen clearance. We have now shown that, no matter what initial encounter the DC has, there exists an ability of CD4 T help to amplify this initial encounter. Using next generation RNA sequencing of DCs receiving innate stimulation with/without T cell-help we have been able to advance our understanding of the way T cell help regulates DC responses. We have elucidated novel transcription factor binding sites regulated by help and not by interferon that maybe involved in help pathways. The identification of genes that are only regulated in DCs receiving innate stimulation when in combination with T cell-help and not either alone has also allowed the investigation of both molecular and cellular phenotypic markers of ‘Helped’-DCs. This novel panel of genes and markers provides us with tools to identify and target DCs to elicit tailored immune responses.