Theory predicts that hosts should evolve highly specific immune defences when there are significant fitness costs associated with parasitic infection. Historically, mechanistic studies have defined invertebrate immunity as innate and non-specific. However, recent evidence from ecological studies challenges this view by finding a high degree of specificity between host and parasite and evidence of immune priming, that are indicative of a more complex system. Critics of the ecological perspective assert that without mechanistic evidence, there is no sound reason to assume that these phenomena are generated by innate immunity. To begin bridging the gap between mechanistic and ecological fields of innate immunity, I have examined the molecular basis of specificity and priming in the model Bombus-Crithidia host-parasite system.\ud My studies show that immune gene expression mirrors the interaction effect found with indirect, ecological measures of immunity, providing unequivocal evidence of innate immune specificity in invertebrates. A similar examination of immune priming suggested that the genes I analysed were not involved in this phenomenom and is most likely to be indicative of the relative importance of different arms of immunity in the primed immune response. Finally, I examined more general aspects of the immune response to Crithidia by characterising the temporal dynamics of immune gene expression throughout infection for the first time in this model host-parasite system. I also confirmed that the assumed link between virulence and intensity of Crithidia infection is valid. To conclude, my studies have shown that integration of molecular knowledge into natural host-parasite systems can only serve to enrich our understanding of the wider capabilities of invertebrate innate immunity
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