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题名: Transgenic overexpression of anti-double-stranded DNA autoantibody and activation of Toll-like receptor 4 in mice induce severe systemic lupus erythematosus syndromes.
作者: Tai-Ping Lee
Shye-Jye Tang
Ming-Fang Wu
Ying-Chyi Song
Chia-Li Yu
Kuang-Hui Sun
贡献者: 國立臺灣海洋大學:生命科學暨生物科技學系
关键词: Lipopolysaccharides (LPS)
Systemic lupus erythematosus (SLE)
Anti-double-stranded DNA autoantibody (Anti-dsDNA)
Single chain variable fragment (scFv)
Toll-like receptor 4 (TLR4)
日期: 2010
上传时间: 2016-09-01T07:00:22Z
出版者: Journal of Autoimmunity
摘要: Abstract: Systemic lupus erythematosus (SLE) is a multi-organ autoimmune disease characteristized by the presence of autoantibodies against double-stranded DNA (anti-dsDNA) in sera at high levels. Bacterial infections in SLE are associated with higher morbidity and mortality. Our goal was to observe the interaction between these 2 factors in the pathogenesis of lupus. We generated transgenic mice with monoclonal anti-dsDNA to investigate the development of lupus. By challenging the mice in vitro and in vivo with Toll-like receptor 4 (TLR4) ligand lipopolysaccharides (LPS), we were able to examine the role of bacterial infection in SLE. In our study, the transgenic mice with a secreted form of anti-dsDNA were found to have higher levels of anti-nuclear antibodies, anti-dsDNA, blood urea nitrogen, and proteinuria. The splenocytes of the mice stimulated with LPS secreted more anti-dsDNA, IFN-γ, and IL-10. After injecting them with LPS in vivo, we further found higher immune complex depositions and IL-10 in the kidneys of the transgenic mice. Moreover, the LPS-injected transgenic mice had higher mortality rate. This is the first transgenic model to demonstrate that only 2 risk factors, pathogenic anti-dsDNA and TLR4 activation, induce severe SLE syndromes in normal mice through the overproduction of IL-10 and IFN-γ. These findings imply that anti-dsDNA and bacterial infections have pivotal roles in the pathogenesis of SLE; the inhibition of TLR4 may be regarded as a therapeutic target.
關聯: 35(4)
URI: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/38436
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