Cutting Edge: Ectopic Expression of CD40 Ligand on B Cells Induces Lupus-Like Autoimmune Disease

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-o...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2002-01, Vol.168 (1), p.9-12
Main Authors: Higuchi, Tetsuya, Aiba, Yuichi, Nomura, Takashi, Matsuda, Junichiro, Mochida, Keiji, Suzuki, Misao, Kikutani, Hitoshi, Honjo, Tasuku, Nishioka, Kiyoshi, Tsubata, Takeshi
Format: Article
Language:English
Subjects:
Animals
Antibodies, Antinuclear - biosynthesis
B-Lymphocytes - immunology
CD40 Ligand - genetics
CD40 Ligand - metabolism
CD40 Ligand - physiology
DNA - immunology
Histones - immunology
Immune Complex Diseases - immunology
Immune Complex Diseases - pathology
Kidney - pathology
Lupus Nephritis - immunology
Lupus Nephritis - pathology
Mice
Mice, Inbred MRL lpr
Mice, Transgenic
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Summary: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.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.168.1.9