My laboratory studies the immunology, genetics and clinical expression of autoimmune diseases. Like most autoimmune disease, systemic lupus erythematosus and Sjögren’s disease predominantly affect women. Understanding the female bias of autoimmune disease at a fundamental level will be a critical step forward.

Antibodies are produced by the immune system against foreign invaders such as bacteria and viruses. In autoimmune disease, antibodies are produced against the self. We study how such antibodies are involved in Sjögren’s syndrome. We produced recombinant, human monoclonal antibodies from B lymphocytes from Sjögren’s patients to study the disease-causing potential of these autoantibodies. Our results indicate that autoantibodies are produced in the salivary glands of Sjögren’s patients. These antibodies can impair saliva production, perhaps by binding muscarinic receptors. Unusual glycosylation of antibodies can also lead to autoimmunity.

Post-traumatic stress disorder is common and associated with an increased risk of autoimmune diseases, including lupus, rheumatoid arthritis, multiple sclerosis and thyroid disease. We also study autoantibodies and B lymphocyte hyperactivity in PTSD. We are working to distinguish if immune abnormalities predispose patients to both PTSD and autoimmune disease, or if PTSD might induce immune system alterations that lead to autoimmunity.

Infection with Epstein-Barr virus (EBV), the causative agent of mononucleosis, may be important in the genesis of lupus and Sjögren’s syndrome. We are determining whether the Epstein-Barr nuclear antigen 2 (EBNA2), a genetic transcription factor, binds to genes that increase the risk of Sjögren’s syndrome. In addition, we will determine whether EBNA2 is expressed in the salivary gland from Sjögren’s patients. These studies should develop a pathophysiological basis by which EBV infection may lead to autoimmune disease.