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• W2410005990 abstract "<h3>Background</h3> Despite growing insights in the breach of immune tolerance, it remains currently unknown which molecules drive or control pathogenic B cells in human rheumatoid arthritis (RA). Recently we have identified a marked increase in expression of the B cell-specific transcriptional co-activator Bob1 in RA synovitis. Additionally, we found that mice lacking Bob1 failed to produce pathogenic anti-collagen autoantibodies and were completely protected from collagen-induced arthritis (CIA), the animal model of RA. <h3>Objectives</h3> We aimed to determine whether this remarkable resistance to CIA in the absence of Bob1 is caused due to lack of functional germinal centers or by intrinsic defects in the B cells of these animals. Furthermore we proceeded to prove that the resistance to CIA is caused exclusively by B cells lacking Bob1. <h3>Methods</h3> First, to determine whether intrinsic B cell defects were the basis of the CIA resistance, we transferred wild type (WT) B cells to Bob1-deficient mice, lacking functional germinal centers (GC), followed by CIA. Then, in order to prove that functional Bob1 exclusively in B cells is required for susceptibility to CIA, we adoptively transferred various combinations of WT and Bob1-deficient B and T cells to RAG-1-<i>null</i> mice followed by CIA induction. <h3>Results</h3> After transfer of WT cells to Bob1-deficient animals, Bob1-deficient mice were still resistant to CIA, suggesting that resistance to CIA is related to GC formation rather to intrinsic B cells defects in the absence of Bob1 and that GCs are important in the pathogenesis of CIA. In the RAG-1-<i>null</i> adoptive transfer model we only observed clinical symptoms of arthritis in the mice that received WT B cells. Moreover, anti-collagen antibodies were only found in the serum of mice that had received WT B cells. Mice lacking Bob1 in their transferred B cells were still protected from CIA. <h3>Conclusions</h3> This data strongly suggest that expression of Bob1 in B cells is indispensable for GC formation and required for the development of CIA and the formation of anti-collagen antibodies. The mechanisms behind an aberrant Bob1 expression and the break of peripheral tolerance in RA is currently under investigation. <h3>Disclosure of Interest</h3> None declared" @default.
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• W2410005990 date "2015-06-01" @default.
• W2410005990 modified "2023-09-27" @default.
• W2410005990 title "OP0295 Mice Lacking Bob1 Exclusively in B Cells are Resistant to Type II Collagen-Induced Arthritis" @default.
• W2410005990 doi "https://doi.org/10.1136/annrheumdis-2015-eular.2679" @default.
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