Shu Man Fu, MD, PhD

Shu Man Fu, MD, PhD

null Shu Man Fu, MD, PhD
Appointment: Margaret M. Trolinger Professor of Rheumatology;
Professor of Internal Medicine and Microbiology
Department of Medicine
Division of Clinical Rheumatology
Conditions Treated: Rheumatology, clinical immunology, systemic lupus erythematosus, rheumatoid arthritis, general rheumatic diseases
Research Description:
Genetic and environmental factors, autoimmunity in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA)


Graduate School: Stanford University, MD; Rockefeller University, PhD
Residency: Internal Medicine, Stanford University and New York Hospital
Certification: Internal Medicine, Rheumatology
Research Interests: Genetic and environmental factors, autoimmunity in systemic lupus erythematosus (SLE) and rhematoid arthritis (RA)

Research Description

Autoimmunity plays an important role in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). The emphasis of my laboratory is on the genetic and environmental factors important for these disorders. We have been focused on the mouse model NZM2328 for SLE. This model was progress to chronic GN and that acute GN and chronic GN are under separate genetic control.

Current efforts are to elucidate the genes controlling these phenotypes. In addition, the hypothesis that molecular mimicry initiates the initial autoimmune response, which diversifies to multiple autoantigen, resulting in end organ damage in suitable hosts is being tested. The role of MHC in this process in both mice and men is being investigated. In this regard, bacterial and viral agents sharing cross reactive T and B cell epitopes with human auto antigens are logical candidates for molecular mimics in this process.

In collaboration, the laboratory is interested in the mechanisms of autoantibody diversification and the role of T cells in the pathogenesis of glomerulonephritis. Recently we have focused our attention on the role of molecular mimicry to environmental antigens at the T cell level in the generation of lupus related autoantibodies. Our laboratory findings let us put forward a new hypothesis on the pathogenesis of SLE.


Selected Publications

PubMed listings for this author >>


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