> Skip repeated content

Mary Kirkland Center for Lupus Research

2003-2006 Kirkland Scholars

Timothy W. Behrens, MD
John F. Finn Professor of Medicine
University of Minnesota
Minneapolis, MN

Dr. Behrens received his medical training at Southern Illinois University, and Internal Medicine residency training at the Medical College of Wisconsin in Milwaukee, where he also was Chief Medical Resident. He performed specialty training in Rheumatology at the Medical College of Wisconsin, and he worked in the laboratory of Dr. James Goodwin, exploring the role of arachidonic acid metabolites on human T and B cell function. He completed additional postdoctoral work at the Metabolism Branch of the National Cancer Institute in Bethesda, MD, where his research focused on the cloning of B cell specific genes. From there, he joined the faculty of the University of Minnesota Medical School, in the Division of Rheumatic and Autoimmune Diseases, Department of Medicine. Dr. Behrens currently serves as Chief of the Autoimmunity Group in the Center for Immunology at the University of Minnesota, and leads the Center for Lupus Research, a newly established multi-disciplinary center bringing together a group of investigators to further the understanding of the genetics and genomics of SLE and other autoimmune disorders.

Dr. Behrens is a leader in the analysis of the human genes that confer susceptibility to SLE. He has one of the world's largest collections of sib-pair, trio and case material for human SLE. His group has performed extensive genome screens in SLE, and more recently has moved to large-scale association methodology to identify genes for systemic lupus. Together with Dr. Peter Gregersen and Dr. Ann Begovich of Celera Diagnostics, Inc., the Behrens laboratory recently identified the protein tyrosine phosphatase PTPN22 R620W allele as an important genetic risk factor in lupus, adding to the evidence that this is a very powerful gene for predisposition to many different autoimmune phenotypes.  Another major effort in the Behrens laboratory is the application of genome-wide gene expression profiling to characterize the peripheral blood RNA expression patterns in lupus and other autoimmune diseases. These studies have successfully identified a strong interferon gene signature in blood cells of lupus patients that correlates with more severe disease and appears to be able to identify those patients with increased disease activity and a greater likelihood for flares and other new events. Finally, the Behrens laboratory has a program in B cell development and biology, where they are using transgenic and knockout mouse models to address the genetics of B cell tolerance and activation. This group is currently interested in the mechanisms that control receptor editing in B cells, the basic biology of class switch recombination, and the role of a novel chemokine receptor in marginal zone B cell function.

Jill P. Buyon, MD
Professor of Medicine, New York University School of Medicine, and Vice-Chairman, Department of Rheumatology, Hospital for Joint Diseases, New York, NY

Dr. Buyon is internationally recognized for her research on neonatal lupus and rheumatic diseases in pregnancy. She is Principal Investigator of a number of recently completed and ongoing NIH-funded research projects, including the multi-center clinical trial "Safety of Estrogens in Lupus Erythematosus National Assessment" (SELENA); the "PR Interval and Dexamethasone Evaluation (PRIDE) in Congenital Heart Block" clinical trial; the U.S. National Research Registry for Neonatal Lupus; and the basic science study, "Maternal Autoantibodies: Pathogenesis of Neonatal Lupus." In addition, Dr. Buyon oversees a number of industry-sponsored clinical trials of new pharmaceutical treatments for lupus. 

Dr. Buyon's commitment is to "translational" research - to translate what doctors learn from treating patients into projects investigated in the laboratory, and then to translate lab findings back to the bedside, in the development of more effective therapies. Previous work by her laboratory has enhanced the ability to identify mothers at greatest risk for having a child with congenital heart block (CHB), a potentially life-threatening problem in some babies born to mothers who have autoantibodies called anti-SSA/Ro-SSB/La. The antibodies and antigens involved have been extensively characterized at the molecular level.  Despite these advances, however, the role of these antibodies in causing cardiac injury is not fully defined. Her laboratory is developing a mouse model of autoantibody-mediated heart block, which will be invaluable in defining pathology and assessing potential therapeutic interventions and preventive strategies. Current focus is on understanding the mechanism by which these autoantibodies initiate a relentless program of fibrosis in the fetal cardiac conduction system. Information on mortality, the need for pacemakers, and recurrence rates in a subsequent pregnancy is critical for family counseling, research strategies and management.

Gary Gilkeson, MD
Professor of Medicine in the Division of Rheumatology
Medical University of South Carolina in Charleston, SC

Dr. Gilkeson is a graduate of the University of Texas, Southwestern Medical School in Dallas and did his Internal Medicine training at UNC, Chapel Hill before completing his fellowship in Rheumatology at Duke University Medical Center. Both his clinical interests and research interests are in lupus nephritis with an emphasis on ethnic disparities in outcomes in lupus in African Americans. His research in African Americans with lupus includes studies of environmental influences on lupus and genetic studies of lupus in the Sea Island African American population in South Carolina, the "Gullahs". His basic research centers on transcriptional factor regulation of inflammatory gene expression in lupus. Lupus is a multifactorial disease, one feature of which is a heightened inflammatory response in the kidney to immune stimuli. Dr. Gilkeson and his group are studying what mediators are important in lupus inflammation, including complement factors and nitric oxide. They are also studying potential mechanisms for the heightened inflammatory response including defects in the intrinsic off signals for inflammation. Finally, his group is active in clinical trials in lupus and he is part of the working group for identifying and developing new biomarkers in lupus. Dr. Gilkeson is currently serving on the Committee on Research for the American College of Rheumatology and is the Chair of the Medical/Scientific Advisory Council for the Lupus Foundation of America.