Dysfunction of the epithelial barrier may lead to Inflammatory Bowel Diseases (IBD), commonly separated into two major diseases: Chron's disease and Ulcerative colitis. We are interested in understanding disease mechanisms that are playing a role in IBD with an emphasis on uncovering the role of hundreds of known risk genes, many of them with unknown function.
We use single-cell genomics, cell-cell interactions, and computational methods to map the risk gene expression across the different cells of the tissue, its cellular context, and its interactions with other cells within the tissue. In parallel, we are utilizing two-component systems such as co-culture of organoids and immune cells to learn more about these interactions and their role in the initiation and progression of IBD.