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Cutting Edge |
*
Department of Immunology, Medical Research Institute, and
Department of Dermatology, Faculty of Medicine, Tokyo Medical and Dental University, Tokyo, Japan;
Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Kyoto, Japan;
Department of Veterinary Science, National Institute of Infectious Diseases, Tokyo, Japan;
¶ Division of Transgenic Technology, Center for Animal Resources and Development, Kumamoto University, Kumamoto, Japan; and
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Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan
CD40 ligand (CD40L) is ectopically expressed on B cells in patients with systemic lupus erythematosus (SLE) and lupus-prone BXSB mice. To assess the role of the ectopic CD40L expression in development of SLE, we have established transgenic mice expressing CD40L on B cells. Some of the 12- to 14-mo-old CD40L-transgenic mice spontaneously produced autoantibodies such as antinuclear Abs, anti-DNA Abs, and antihistone Abs. Moreover, approximately half of the transgenic mice developed glomerulonephritis with immune-complex deposition, whereas the kidneys of the normal littermates showed either no pathological findings or only mild histological changes. These results indicate that CD40L on B cells causes lupus-like disease in the presence of yet unknown environmental factors that by themselves do not induce the disease. Thus, ectopic CD40L expression on B cells may play a crucial role in development of SLE.
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