Investigating the functional basis of shared genetic aetiology across autoimmune diseases

Autoimmune diseases are thought to arise when cells of the immune system, which normally fight off infections, become inappropriately activated and instead mount a response against the body leading to pervasive tissue damage. These diseases, which include conditions such as multiple sclerosis, type 1 diabetes, rheumatoid arthritis and inflammatory bowel disease, are estimated to afflict about 10% of the population worldwide. They pose a substantial personal and socioeconomic burden and they have no cure. There is a fundamental need to develop improved therapeutic strategies to treat these diseases through an optimal modulation of the immune system that allows substantial symptom alleviation but without leading to the severe or even fatal side-effects that can occur with currently available treatments.

Interrogating the biological consequences of genetic factors that contribute to the development of multiple autoimmune conditions provides an approach that can uncover the key mechanisms that underpin these diseases. I will investigate the basis of shared genetic risk across different autoimmune conditions at the molecular level and determine the downstream cellular changes arising due to the genetically determined molecular differences and help define key disease pathways. I will also investigate the best way to regulate key disease pathways.