Human beings vary in how their immune systems functions: some of us recover more rapidly from infections, react more violently to foreign objects, or take longer for inflammation to go down. We also vary in our risk of developing more serious diseases of the immune system, such as inflammatory bowel diseases, or multiple sclerosis. Both healthy variation and risk of disease are partly driven by differences in our DNA, and this common genetic cause can help us understand how the two are related.
Over the last 10 years our understanding of the genetics of immune diseases has increased immesurably, and my PhD was spent discovering and characterising the genetic basis of inflammatory bowel diseases (such as Crohn's disease). However, the next major challenge is to understand the specific changes in the immune system that these genetic differences are causing.
To this end I develop statistical techniques to jointly analyse data from different immune diseases, and combine it with measurements of the immune system of patients. These techniques include Bayesian multinomial methods, as well as model selection methods to partition up genetic risk into pathways and line these up with variation in intermediate phenotypes. I also collaborate with scientists around Oxford and internationally to develop and interpret new datasets for understanding the immune system.