Crohn's disease and ulcerative colitis, two forms of Inflammatory Bowel Disease (IBD), are disorders believed to be caused by the cells of the immune system mistakenly attacking the tissues of the digestive tract. This phenomenon, known as autoimmunity, leads to massive inflammation of the affected area and consequently causes severe pain, diarrhea, bleeding and other debilitating symptoms. With few treatments and no cure to date, this disease continues to impact both the general population and our health care system. Current research suggests that the inflammation associated with IBD is caused by self-reactive immune cells called T cells that attack the gut tissue, along with a loss of T regulatory cells (Tregs), which act to 'turn off' the immune system. Furthermore, flagellin, a protein present on all motile bacteria including the microflora found within the intestine, may also contribute to the establishment of IBD associated inflammation through its influence on T cells and Tregs. Indeed, studies have shown an immune response is generated against flagellin in 50 percent of patients with Crohn’s disease. However, the nature of these responses remain largely uncharacterized. Megan Himmel's research aims to optimize a novel method of identifying T cells and Tregs which are specifically reactive to flagellin, in order to study their function and their possible contribution to the pathogenesis of IBD. This work may lead to a novel diagnostic marker for IBD, as well as further insight into the immune mechanisms contributing to this disease. Furthermore, Ms. Himmel’s research will provide important insight into the overall role of T cells and Tregs in the establishment and progression of IBD in humans, with the ultimate goal of establishing methods to therapeutically manipulate the balance of pathogenic versus regulatory immune responses.