Research interests

My immunological research takes the stand that, people with altered immune function have an increased risk of developing cardiac diseases due to cell-mediated inflammation, immune complex-mediated inflammation and autoantibody-mediated inflammation. Immune system function can be affected by many factors, such as stress, disease, aging, or drugs. I plan to focus on two of the most common afflictions, autoimmune disease and aging. Currently, nearly 40% of the world’s population is affected by one or both of these afflictions. Decreased immune function is not caused by an overall decrease in cell population, but a shift from healthy non-autoreactive cells to unhealthy autoreactive problem causing cells. For example, in mice and humans experiencing either autoimmune disease or the effects of aging, B1b lymphocyte populations are increased. B1b lymphocytes differ from normal B lymphocytes. B1b lymphocytes do not progress through B lymphopoiesis as their normal counterparts do, due to alterations in the signaling mechanisms driving B lymhopoiesis. This results in hyperactive lymphocytes that are prone to attacking self antigens (one’s own body). These same phenomena; increased B1b lymphocyte populations and autoimmunity, occur in mice having partially inactive Tetratricopeptide Repeat Domain 7 (Ttc7) protein. Through this research I intend to uncover the signaling mechanisms behind the switch from normal B lymphocyte production to B1b lymphocyte production through the study of the transcirptional control of Ttc7. I am looking to discover the cellular processes that become altered to produce dysfunctional immune cells that attack the self causing autoimmune and cardiovascular diseases.