Our research is integrated within the broader theme of understanding the homeostasis of type I interferon (IFN-I) signalling and the pathogenic consequences of aberrant recognition of self-derived nucleic acids. Within this framework, my group focus on how dysregulated innate immune sensing—particularly of mitochondrial nucleic acids—drives human autoinflammatory diseases such as neuroinflammation and lupus. We also investigate whether breaks in tolerance to mitochondrial nucleic acids contribute to inflammation and pathogenesis in mitochondrial disorders. By leveraging insights from rare Mendelian diseases and patient cohorts, our work aims to uncover fundamental principles of immune regulation with direct relevance to both rare and common inflammatory conditions.