My work focusses on understanding how the genetic variation underlying complex disease impacts immune-function. I am passionate about operating on the intersection of computational and cellular biology, as I believe this is where the potential for mechanistic insight lies.
Our work focusses on studying how the genetic basis for complex immune mediated disease impacts the function of T cells. To do this we use computational screens as a starting point for subsequent in vitro follow up. This approach allows for directly assaying the role of immune disease genes in modulating distinct cellular phenotypes, thereby providing mechanistic insight into the role of these immune disease genes. This is done by introducing edits into these target genes thereby rendering the target gene unfunctional. Subsequently, the effects of the edits on T cell function can be identified. Given the direct link to disease, the hope is that such genes will be actionable therapeutic targets for the associated disease. My role is in designing and executing the computational aspects, as well as thinking along with the design of the wet-lab experiments. This constant feedback loop between wet and dry lab is essential for generating robust and interpretable data.
While my PhD period focussed on the computational aspects of studying immune function and complex disease, a key area where I would like to develop over my post-doc is the design of these in vitro experiments. This is what attracted me to the Sanger and the Trynka group, as there is a lot of interdisciplinary expertise on immunology, computational and cellular biology. This unique environment allows for integrating the best of high throughput of computational analysis with the key insights gained form bespoke cellular assays, which is where I believe the greatest potential for actionable insight lies.