The central hypothesis of our laboratory is that commensal microbes at the intestinal mucosal surface modulate local adaptive immune responses that affect the development of autoimmunity. We utilize a diversity of research methods from animal models to human tissues, as well as participate in a larger, highly-collaborative environment that includes individuals from rheumatology, gastroenterology, immunology, microbiology, molecular biology, and biochemistry. We have utilized biospecimens from individuals with Inflammatory Bowel Diseases like Crohn's and Ulcerative Colitis, Spondyloarthritis, and Rheumatoid Arthritis to identify unique bacterial and metabolic signatures that influence immune functions. We also integrate murine models of autoimmune arthritis and bowel inflammation into our work. Our group has developed methods of isolating, identifying, and transferring primary bacterial strains from mice and humans with disease into germ free mice to interrogate the immunologic consequences. More recently we have developed methods to manipulate bacterial metabolism in mice to investigate the impacts on immune functions. These models have become central to taking our observations from human to mechanistic investigations into how specific commensal bacteria affect adaptive immunity in autoimmunity.