Dr Gosia Trynka

Gosia leads the immune genomics group who study how human genetic variation impacts immune system and predisposes to development of autoimmune diseases.

I strongly believe that interdisciplinary approaches are essential to achieve meaningful insights into biological processes. The combination of molecular techniques, genomic assays, and computational methods that we develop and apply to study the immune system is a reflection of my own career path through several disciplines within biology and genetics.

With a backround in molecular biology, I became interested in medical and population genetic approaches to study genetic determinants for immune related diseases. I joined Prof. Cisca Wijmenga's group where I was a co-lead analyst for the genome-wide association study (GWAS) and an Immunochip study for coeliac disease (an immune disease of the small intestine resulting from intolerance to gluten). These studies resulted in identification of tens of disease risk loci and pointed to strong shared genetic backround between celiac disease and a range of other common immune conditions, including type-1 diabetes, rheumatoid arthritis, and inflammatory bowel disease.

Despite our great success in mapping disease risk variants, I was disappointed by the limited insights that we gained in understanding biology of complex immune diseases. I therefore carried out my postdoctoral research at Brigham and Women's Hospital, Harvard Medical School and Broad Institute where I joined Dr. Soumya Raychaudhuri's and Dr. Robert Plenge's groups. I invested my time in developing statistical methods that allow translation of GWAS associations into biological functions. By integrating disease-associated variants with functional genomics data, these approaches pointed to specific cell types being relevant in the pathogenesis of numerous complex traits, including immune diseases. My group at the Sanger Institute continuous with experimental and computational efforts to further map and translate immune disease genetic variants to function.