The cause of autoimmunity is not fully understood. A current paradigm proposes that complex interactions between genetic and environmental factors result in a break in immune tolerance (ie. the ability of the immune system to delineate foreign from self antigens) and the generation of autoreactive T cells, autoreactive B cells and autoantibodies that cause autoimmunity.
Our lab is interested in understanding the cellular and molecular mechanisms by which CD4+ T helper (Th) cells, a integral part of the adaptive immune system and the bodies ability to fight infection, become dysregulated and cause sterile inflammation.
To do this we pair basic research studies in experimental mouse models of arthritis and uveitis with clinical studies done with blood samples from patients with rheumatoid arthritis, ankylosing spondylitis, and Blau Syndrome to answer the following questions:
How do microbial sensors including pattern recognition receptors control autoreactive CD4+ T cell responses that cause arthritis and uveitis?
What are the cellular mechanisms by which single point mutations in the gene NOD2 cause the human monogenetic inflammatory disease Blau Syndrome?
How do fungal infections control autoimmunity? What host factors regulate both anti-fungal immune responses and autoimmunity?