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- W2075330716 abstract "Self-specific B cells play a main role in the pathogenesis of lupus. This autoimmune disease is characterized by the generation of autoantibodies against self antigens, and the elimination of B and T cells involved in the pathological immune response is a logical approach for effective therapy. We have previously constructed a chimeric molecule by coupling a DNA-mimotope peptides to an anti-CD32 antibody. Using this protein molecule for the treatment of lupus-prone MRL/lpr mice, we suppressed selectively the autoreactive B-lymphocytes by cross-linking B cell receptors with the inhibitory FcγRIIb receptors. This approach was limited by the development of anti-chimeric antibodies in MRL mice. In order to avoid this problem, we established a murine severe combined immunodeficiency lupus model, allowing a long-term chimera therapy. Elimination of the double-stranded DNA-specific B cells by chimera therapy in MRL-transferred immunodeficient mice resulted in inhibition of T cell proliferation and prevented the appearance of IgG anti-DNA antibodies and of proteinuria." @default.
- W2075330716 created "2016-06-24" @default.
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- W2075330716 date "2014-02-06" @default.
- W2075330716 modified "2023-10-01" @default.
- W2075330716 title "Suppression of dsDNA-specific B lymphocytes reduces disease symptoms in SCID model of mouse lupus" @default.
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- W2075330716 doi "https://doi.org/10.3109/08916934.2014.883502" @default.
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