Malaria is responsible for over 500.000 deaths every year, mostly of young children. For this reason there is a high medical need for a protective vaccine. Intravenous injections with radiation-attenuated sporozoites isolated from mosquito salivary glands have been shown to provide such protection against malaria in mice and humans by preventing parasite progression from liver to blood stage. Unfortunately, obtaining the currently required amount of sporozoites from mosquito salivary glands is too cumbersome for routine use in places where the vaccine is most needed. Therefore, alternative protocols aimed at increasing sporozoite immunogenicity during T cell priming and subsequently during expansion and differentiation in the liver are warranted. Immunization with radiation-attenuated sporozoites has been shown to induce responses by various CD8+ T cell subsets. In particular, high frequencies of liver resident memory CD8+ T cells correlate with protection. We recently showed that innate sensing of plasmodium nucleic acids also contributed to restricting plasmodium replication in the liver. In this project, we evaluate whether agonists of innate nucleic acid receptors can be exploited as adjuvants during radiation-attenuated sporozoite vaccination protocols in the murine model of Plasmodium berghei ANKA liver stage infection. Preliminary results suggest that the activation of TLR9, TLR7, RIG-I and cGAS sensors by our selected agonists induces the production of the pro-inflammatory cytokine IFN‑α, detected mainly in serum and spleen of B6 mice. Interferon stimulated genes, especially IFIT1, and the cytokine IFN-β were highly up-regulated in spleen and liver after stimulation of the nucleic acid sensors. As a proof-of concept, high frequencies of resident memory CD8+ T cells were found in livers of immune mice with normal endogenous TCR repertoire. Additionally, efficient protocols for the generation of effective RAS were established.