Our MissioN

general public

Our lab studies some of the ways that the immune system keeps itself under control, and diseases that happen when it fails to do that task well. You may know someone who has one of these conditions: asthma, food allergy, chronic infections, rheumatoid arthritis, type 1 diabetes, multiple sclerosis, Grave's thyroiditis, lupus, autoimmune retinopathy, or autoimmunity directed at other organs of the body. All of these are examples of the immune system not being regulated properly. Our research focuses on a particular group of cells in the immune system that we think plays a very important role in controlling the development of these diseases...killer B lymphocytes.   

medical researchers

Our primary goal is to improve treatment of autoimmune and inflammatory diseases by targeting antigen-specific T cells using regulatory antigen presenting cells, particularly killer B cells that express the death-inducing molecule, Fas ligand. Developing immature T cells have random specificities, including reactivity to self antigens that have the potential to cause autoimmune diseases. These self-reactive T cells are supposed to be deleted, made anergic, or turned into regulatory T cells during the process of central tolerance in the thymus. To further protect the individual, other mechanisms including cell death mediated by cells expressing Fas ligand exist that are capable of removing self-reactive T cells in the periphery (peripheral tolerance). Unfortunately, people with certain genetic predispositions or environmental pressures do not tolerize their self-reactive T cells properly, and therefore, have greatly increased risks of developing autoimmunity. Our current goal is to tip the balance in favor of peripheral tolerance by stimulating one of the natural mechanisms of T cell control, Fas ligand expression by antigen presenting B cells. We believe that regulatory B cells expressing death-inducing ligands or suppressive cytokines such as IL-10 and TGF beta hold great promise in delivering tolerizing signals to the T cells that cause autoimmunity. Similarly, T cells that recognize otherwise innocuous allergens are involved in the pathogenesis of asthma. Removing or regulating the allergen-specific T cells by similar methods as those described for autoimmunity is likely to have clinical benefit.