Harini Bagavant, MBBS, PhD
Degree(s): MBBS, PhD
Graduate School: National Institute of Immunology, New Delhi
Primary Appointment: Associate Professor, Medicine, Nephrology
Pathogensis of lupus glomerulonephritis in murine models of Systemic Lupus Erythematosus
Email Address: hb5u@Virginia.edu
Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease characterized by circulating autoantibodies to nuclear and cytoplasmic antigens and involves multiple organ systems like kidney, skin, heart, and brain. The primary focus of my research is to investigate the pathogenesis of renal disease in lupus using murine models of spontaneous SLE. The renal involvement or lupus glomerulonephritis is associated with deposition of immune complexes and complement in the glomeruli, inflammation, and progressive loss of renal function resulting in renal failure, a significant cause of morbidity in patients with SLE.
The mechanisms underlying initiation and progression of renal disease in SLE are not completely understood. Although autoantibodies deposited in the kidneys and their target antigens have been investigated extensively as the primary basis of renal pathology in SLE, there is significant evidence for the role of other immune mediators in this process. Using different murine models, we have shown that presence of serum autoantibodies and glomerular immune deposits is not sufficient to cause renal failure in lupus-susceptible strains. Our studies indicate an important role for pathogenic autoreactive T cells as key players in lupus nephritis. In addition to the autoimmune responses, we are also interested in the investigation of factors intrinsic to the renal cells influence progression of glomerular pathology. Strategies to modulate the local inflammatory responses in the kidney as a therapeutic approach are under investigation.
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