Systemic lupus erythematosus is a common, debilitating autoimmune disease in which components of the body’s own cells are targeted and attacked by the immune system. The origins of the disease are still unclear, but it is known that genetic, environmental, and hormonal factors are all involved in causing lupus. We are studying the molecular mechanisms of genetic risk factors and how they contribute to lupus.
Although there is a strong genetic component to lupus, not much is known about how genes influence the development of the disease. We are focusing on lupus-associated variations in the IRF5 gene. The IRF5 protein is a key intermediary in the response to viral infection. People with lupus tend to have certain variations in their IRF5 gene, that cause it to be either expressed at a higher level or spliced differently than in people without lupus. We hypothesize that the modifications to the IRF5 gene associated with lupus leads to increased interferon production and disruption of several cellular pathways. This disruption results in the production of antibodies against normally occurring parts of cells and can lead to lupus. Through studying these interactions, we hope to identify markers for people who are at high risk for lupus, and early indicators that autoimmunity is developing. Early intervention in the disease has shown promise in slowing its effects. We also hope to evaluate the role of interferon in lupus and evaluate the potential of blocking interferon as a treatment for the disease.
Another interest of our laboratory is virology, especially Epstein-Barrvirus and Herpes Simplex virus. We are currently exploring how infection with these viruses affects gene expression in the infected cells.