Dylan Spitalnick

Inflammatory Bowel Disease (IBD) is a category of chronic, autoimmune disease that induces inflammation in the gastrointestinal tract of approximately 1.6 million people in the United States. One factor in IBD pathology is the gut microbiota (collection of microorganisms in the gut), which has been heavily studied due to its significant influence on IBD development and its potential therapeutic value. The gut microbiota performs various functions, from helping with food digestion to regulating the immune system.

The intestinal epithelium is the outermost layer of the intestine and is your body's first layer of defense against disease-causing pathogens. In IBD patients, the epithelium is more permeable than normal, allowing for more pathogens to easily infiltrate the body. One type of important immune cell which resides in the epithelium, intraepithelial lymphocytes (IELs), are crucial for repairing the epithelium and further protection against this infiltration. However, in IBD patients, IEL behavior can be altered and they often lose these beneficial functions.

Recently, researchers identified a special type of mouse with a unique microbiota where a specific subset of IELs, γδ (gamma delta) IELs, were increased. While this increase in γδ IELs has been identified, it is unclear how other immune cells are affected in the phenotype. My study will be looking at how macrophages, a prevalent immune cell in IBD, are affected in mice with this phenotype. I will do this by taking samples from the intestines of the special mice and using a technique with antibodies that allows me to see how macrophages and γδ IELs are interacting under a microscope. I will do the same with normal mice and compare the activity and count of the macrophages between them. By better understanding how other immune cells are affected, we can further identify why γδ IELs are increased in this phenotype. This knowledge on how γδ IELs and IELs in general are influenced can help researchers better understand IBD pathogenesis and develop better therapies.