Biography: I’m a research scientist focused on immunology, genetics, and genomics. I aim to use new technologies to unlock the mysteries of inflammatory diseases and find new curative treatments. My research is a mixture of experimental and computational work with large-scale human datasets. I obtained my PhD at the University of Toronto and continued my post-doctoral training at Brigham and Women’s Hospital. I started my independent research group at Cincinnati Children’s Hospital Medical Center in November of 2023.
My interest in autoimmunity work stems from my training and a deep desire to better understand the immune system and how its dysregulation leads to disease. I have an overwhelming need to push scientific boundaries! My research goals are to broadly better understand gene regulation in T and B cells, finding and validating causal autoimmune variants, developing new experimental and computational single-cell tools, and using cutting-edge genomic editing technologies to drive our understanding and treatment of autoimmune diseases.
Research Summary: Juvenile Idiopathic Arthritis (JIA) is the most common autoimmune disease in children. If untreated, it can cause irreversible joint damage and long-term disability. From family studies, we know that siblings and relatives of children with JIA are more likely to develop disease. Previous research has identified this genetic contribution and found many changes in the DNA of affected children. However, the function of these changes and their role in disease is still unknown.
Although current drugs can be effective, over 30% of children JIA will continue to experience uncontrolled symptoms requiring the use of multiple treatments. Finding strategies to predict drug responses and design better therapies is essential to helping children with this devastating condition. In JIA, immune cells in the joint cause irreparable tissue damage. This includes T cells which can either support other destructive cells or directly damage tissue. Unfortunately, previous work has not been able to identify the exact T cells that cause disease. This is because inflamed joints are not biopsied for study. In this proposal, we will use cutting edge technology to identify these disease-causing T cells in the joints of children with JIA.
We will then confirm how changes in the DNA are creating these abnormal T cells. In this way, we hope to identify ways to better predict drug responses and shed light on this complex condition.
