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Rheumatology 2000; 39: 18-27
© 2000 British Society for Rheumatology

Reviews

Systemic lupus erythematosus—messages from experimental models

M. L. Stoll and J. Gavalchin

Division of Hematology/Oncology, Department of Medicine, SUNY Health Science Center at Syracuse, Syracuse, NY, USA

Correspondence to: J. Gavalchin, Department of Medicine, SUNY HSC at Syracuse, 750 East Adams Street, Syracuse, NY 13210, USA.


   Introduction
 
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of autoreactive T cells and autoantibodies that can affect virtually every organ system. The most severe clinical manifestations include immune complex-mediated glomerulonephritis, arthritis, vasculitis, cerebritis, pericarditis, cytopenias and serositis [1]. The diversity of clinical manifestations and disease phenotype, together with limited access to patient tissues, has made the study of human lupus difficult. However, the availability of a number of animal models for SLE has allowed us to make significant progress towards understanding the pathogenetic mechanisms contributing to disease development, and developing therapeutic strategies that specifically target the critical immune cells that are involved. This review will summarize some of the findings in the experimental murine models for SLE that have led to our current understanding of the pathogenetic mechanisms involved in the development of the disease in humans.


   Experimental models for systemic lupus nephritis
 
Spontaneous models
Initial efforts to identify pathogenetic mechanisms in . . . [Full Text of this Article]

Induced models
Transgenic and knockout models

   Immunopathogenesis of SLE
 

   Conclusion
 

   References
 

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