期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 38, 期 12, 页码 3487-3498出版社
WILEY
DOI: 10.1002/eji.200838604
关键词
Autoimmunity; Innate immunity; Lupus; Lupus nephritis; TLR
类别
资金
- Deutsche Forschungsgemeinschaft [AN372/9-1, GRK 1202, SE888/4-1]
- Else Kroner-Fresenius Foundation
Certain viral nucleic acids aggravate autoimmunity through nucleic acid-specific TLR. Viral 5'-triphosphate RNA (3P-RNA) and double-stranded non-CpG DNA induce antiviral immunity via TLR-independent pathways but their role in autoimmunity is unknown. Transient exposure of 16-wk-old MRLlpr/lpr mice to 3P-RNA aggravated lupus nephritis by increasing IFN signaling and decreasing CD4(+)CD25(+) T cells. By contrast, transient exposure to non-CpG DNA exacerbate lupus nephritis in association with splenomegaly, lymphoproliferation, hypergammaglobulinaemia. and increased B220(+)CD138(+) plasma cells. Both, 3P-RNA and non-CpG DNA increased glomerular complement factor C3c deposits but both nucleic acid formats were less potent in aggravating renal pathology as compared with CpG DNA. 3P-RNA and non-CpG DNA also localized to the glomerular mesangial cells and activated cultured mesangial cells to produce IL-6. We conclude, 3P-RNA or non-CpG DNA both trigger autoimmune disease in MRLlpr/lpr mice by specifically activating adaptive immunity but similarly enhance inflammation on the tissue level.
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