Development of safe and effective mucosal vaccines against respiratory pathogens has largely been hampered by the lack of a suitable mucosal adjuvant. We have explored the use of intranasally administered innate-like lymphocyte (ILT) agonists as a novel class of adjuvant to promote adaptive immune responses in the lung. We have shown that stimulation of natural killer T (NKT) cells with the agonist α-galactosylceramide (α-GalCer), or mucosal-associated invariant T (MAIT) cells with the agonist 5-(2-oxopropylideneamino)-6-d-ribitylaminouracil (5-OP-RU), results in activation of dendritic cells (DCs) in the lung tissue and lung-draining lymph nodes. Mechanistically, DCs acquire and present the agonists, facilitating reciprocal “licensing” interactions with ILTs that enhance their stimulatory capacity. Accordingly, co-administration of protein antigens with either agonist by the intranasal route promoted antigen-specific immune responses, although the phenotype of T and B cell responses induced was distinct. We hypothesise that MAIT and NKT cells provide unique licensing signals to DCs, which in turn, alter the adaptive immune response generated. To explore this, we performed single-cell RNA sequencing on purified DC populations from the lung-draining lymph nodes 36 hours after intranasal administration of α-GalCer or 5-OP-RU. Our results show that activating the different ILT populations leads to unique transcription profiles in the DCs, and we are currently mining this data to define the different molecular pathways stimulated. Ultimately this information will shed light on ILT-derived signals that shape adaptive immune responses, and may provide insight on how to exploit this activity in the design of mucosal vaccines.