Interferon alfa and beta receptor confers resistance against Neospora caninum infection in mice

Neospora caninum is an intracellular protozoan that is the causative agent of neosporosis, a disease relevant to the veterinary field for causing neuromuscular disease in dogs and repeated abortions in ruminants. In the present moment, there are no therapies that are able to induce sterile cure against the infection and prevention strategies rely only in environmental management. In this context, we aimed to determine the protective role of the Interferon alpha and beta receptor (IFNAR) during an experimental infection with N. caninum. We performed in vivo experiments with genetically deficient mice (Ifnar^-/-). Those mice, in direct comparison with wildtype (WT) controls, presented reduced survival against the infection, associated with increased parasite load and inflammation in different tissues. In agreement, we observed that the absence of the IFN-I receptor led to a significant reduction in crucial inflammatory mediators that control the infection, namely IL-12, IFN-γ and nitric oxide. Together, our results showed that IFNAR is a central molecule that mediates host resistance against N. caninum by controlling acute and chronic parasite replication, through the induction of an effective Th1 immune response against this protozoan parasite.