David B. Lewis, M.D.
Dr. David Lewis is an Associate Professor of Pediatrics at Stanford University School of Medicine and Director of the Jeffrey Modell Center for Primary Immunodeficiency at Stanford. He received his medical degree at the University of California at San Francisco, and pursued pediatric residency training at the institution and the University of Washington, Seattle, WA. He completed a fellowship in Pediatric Infectious Diseases at the University of Washington, where he remained as a faculty member until 1997, when he joined the Stanford University faculty. Dr. Lewis has a long-standing interest in developmental and genetic limitations in T-cell immunity, including in humans. He is particularly interested in limitations in immunity mediated by CD4 T cells and how this compromises host defenses against intracellular pathogens. As part of his activities with the Modell Center, Dr. Lewis spends about 25% of his time seeing patients with primary immunodeficiencies.
Dr. Cornelius Boerkoel is an Assistant Professor of Human Genetics at Baylor College of Medicine. He received his medical degree and Ph. D. from Case Western University, Cleveland, OH. Following completion of a pediatric residency at the University of Washington, Seattle, WA, he completed a fellowship in Clinical Genetics at The Hospital for Sick Children and the University of Toronto, Toronto, Canada. He then completed postdocatoral research training at Baylor College of Medicine and remained as faculty in the Department of Molecular and Human Genetics. Dr. Boerkoel has a longstanding interest in inherited human diseases, and as part of his activities, Dr. Boerkoel spends approximately 25% of his time seeing patients with inherited disorders. He began his studies of Schimke immuno-osseous dysplasia (SIOD) in 1997. SIOD is characterized by skeletal dysplasia, progressive renal failure, and T-cell immunodeficiency. Additional but more variable disease features include arteriosclerosis, hypothyroidism, and tooth and pigmentary abnormalities. SIOD is usually fatal within the first two decades of life because of renal failure, infection, bone marrow failure, or cerebral ischemia. Dr. Boerkoel's challenge is to explain how mutations of SMARCAL1 cause this severe pleiotropic disease, identify potential therapies to treat or ameliorate the disease, and derive insights into general principles of developmental biology and pathophysiology. To accomplish this, he and his co-workers are using a combination of patient studies, Drosophila and murine genetics, and cell culture systems.