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Research | Core Facilities | Patient Studies | Tech Transfer | Seminars | Intranet | Careers | Search | Contact Us | Ways To Give HOME |
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More about Dr. James 101 COBRE on Science in a Culture of Mentoring Arthritis and Immunology Research Program
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Research Interests Systemic lupus erythematosus is an autoimmune disease which is characterized by the production of high levels of autoantibodies. Our work on the immunochemistry of lupus autoantigens provides the basis for our ongoing research efforts. These epitope mapping experiments led to our peptide induced model of lupus autoimmunity. Genetic analysis of responder and non-responder strains have shown linkage and association with CD72, a polymorphic B cell marker involved in negative regulation of B cells in mouse and man. Using CD72 congenic mice and a large collection of well-characterized human SLE patients, our research efforts now focus on further understanding the role of CD72 in murine models and human SLE. In addition, our laboratory is interested in understanding the pathogenic mechanisms of SLE epitope spreading. Serial serum samples from the Department of Defense Serum Repository show that autoantibodies precede clinical lupus and ongoing work focuses on understanding what specific features of antibodies might change in patient sera at the time of clinical SLE onset. Identification of early humoral autoimmune responses could potentially lead to cross-reactive structures from environmental pathogens which could trigger autoimmunity in susceptible individuals. This approach led to our identification of Epstein-Barr nuclear antigen-1 as the heteroimmune response out of which select aspects of lupus autoimmunity arises. Ongoing research focuses on understanding how such a common infectious agent could be related to such an uncommon disease. We are applying the lessons from SLE to other autoimmune rheumatic diseases, such as scleroderma. The unifying theme of our research efforts is to understand the etiology and pathogenic mechanisms of systemic autoimmune, rheumatic disease. We use antigenic structure to introduce us to the critical molecular elements of the autoimmune process. By applying this information to human disease states, we hope to develop better diagnostic approaches and therapeutic interventions, as well as to contribute to the understanding of basic immune function. Joined OMRF Scientific Staff in 1994. Mailing Address
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