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• W2018087056 abstract "Whereas the role of immune complexes in mediating renal cell and immune cell activation is well established, the contribution of sequence-specific immunomodulatory actions of the chromatin part remains unclear. Toll-like receptor-9 (TLR-9) mediates immunostimulatory effects of unmethylated microbial CpG-DNA. It was hypothesized that hypomethylated CpG-DNA in vertebrates may have similar effects and may contribute to disease progression in lupus nephritis. A synthetic G-rich DNA, known to block CpG-DNA effects, was used in this study. In macrophages, G-rich DNA suppressed CpG-DNA–but not LPS-induced production of CCL5 in a dose-dependent manner. Injections of G-rich DNA suppressed lymphoproliferation induced by CpG-DNA injections in mice. In MRLlpr/lpr mice with lupus nephritis, labeled G-rich DNA co-localized to glomerular immune complexes and was taken up into endosomes of TLR-9–positive infiltrating macrophages. Eleven-week-old MRLlpr/lpr mice that received injections of either saline or G-rich DNA for 13 wk revealed decreased lymphoproliferation and less autoimmune tissue injury in lungs and kidneys as compared with saline-treated controls. G-rich DNA reduced the levels of serum dsDNA-specific IgG2a as well as the renal immune complex deposits. This was consistent with the blocking effect of G-rich DNA on CpG-DNA–induced proliferation of B cells that were isolated from MRLlpr/lpr mice. As oligodeoxyribonucleotide 2114–treated MRLlpr/lpr mice were not exposed to exogenous CpG-DNA, these effects should relate to a blockade of CpG motifs in endogenous DNA. It is concluded that adjuvant activity of self-DNA contributes to the pathogenesis of lupus nephritis. Modulating the CpG-DNA–TLR-9 pathway may offer new opportunities for the understanding and treatment of lupus." @default.
• W2018087056 created "2016-06-24" @default.
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• W2018087056 date "2005-11-01" @default.
• W2018087056 modified "2023-10-18" @default.
• W2018087056 title "G-Rich DNA Suppresses Systemic Lupus" @default.
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• W2018087056 doi "https://doi.org/10.1681/asn.2005060658" @default.
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