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- W82729155 abstract "Abstract We have found dramatically elevated levels of activation-induced cytidine deaminase (AID) in the B cells of generalized autoimmune BXD2 mice that develop spontaneous erosive arthritis and glomerulonepheritis. Pathogenic autoantibodies cloned from these mice exhibit extensive somatic hypermutation and the majority of them have undergone class-switch recombination, suggesting that AID activity plays an important role in the production of pathogenic autoantibodies. Sera from BXD2 mice exhibited significantly elevated IL-17, but not IFN-γ or IL-4, compared to B6 mice. FACS analysis indicates that CD4 T cells in BXD2 mice are preferentially polarized to Th17 cells and these cells also express the early activation marker, CD69, in vivo in BXD2 mice. The B cells from BXD2 mice express high levels of IL-17 receptor (IL-17R) and immunohistochemistry staining shows that B cells are in close contact with the IL-17+ cells in the spleen. Administration of AdIL-17 to 1-mo-old B6 and BXD2 mice induced the expression of AID, promoted development of GCs, and enhanced the sera titers of antibodies. In contrast, administration of AdIL-17R:Fc to 10-mo-old BXD2 mice suppressed the expression of AID, down-modulated the percentage of PNA+Fas+ GC B cells, and suppressed the sera titers of antibodies. Our results provided a unique pathogenic function of IL-17 in that it positions IL-17 as a critical cytokine that regulates GC B cell response and the production of pathogenic autoantibodies." @default.
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- W82729155 date "2007-04-01" @default.
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- W82729155 title "IL-17 promotes germinal center response and AID-regulated pathogenic autoantibody production in autoimmune BXD2 mice (130.21)" @default.
- W82729155 doi "https://doi.org/10.4049/jimmunol.178.supp.130.21" @default.
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