The Kissler lab investigates the causes of autoimmunity. Our goal is to devise a successful strategy to prevent or cure type 1 diabetes.
Collaborative efforts by international consortia over that past decade have yielded an impressive amount of new data on the genetic basis of autoimmunity. So-called genome-wide association studies (GWAS) have identified numerous regions in the human genome that modify the risk of autoimmune disease. But all this new information falls short of explaining how genes contribute to disease. Knowing which genes are involved is insufficient. We now need to understand by which mechanism these genes increase the risk of autoimmunity. To achieve this, we have investigated the function of several key disease genes in mice. In past studies, we have used RNA interference to modify gene activity in a mouse model for type 1 diabetes. We have targeted Slc11a1, Ctla4, Il17, Ptpn22 and Rgs1. We now also use the latest genome editing methods, including CRISPR-Cas9, to target additional genes of interest.
Because disease-associated genes are involved in many different aspects of immunity, our laboratory has studied various facets of the immune system though our work mostly relates to T cell biology. Current research is focused on the regulation of T cell activity by cell-intrinsic mechanisms and by regulatory T cell subsets. By studying disease-associated genes, we have identified pathways not previously linked with autoimmunity that we are now investigating in more depth. Ultimately, we aim to uncover a disease mechanisms amenable to manipulation for the prevention or abrogation of autoimmunity.
Our research is supported by a Career Development Award from the Juvenile Diabetes Research Foundation (JDRF).
Page last updated: September 24, 2018