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The double-stranded DNA (dsDNA)-specific B cell receptor (BCR) is a membrane-bound immunoglobulin expressed on the surface of B cells that specifically recognizes and binds to dsDNA. These receptors are central to the development of anti-dsDNA antibodies, which are hallmark autoantibodies in systemic lupus erythematosus (SLE) and related autoimmune diseases. Upon antigen binding, these receptors initiate signaling cascades leading to activation, proliferation, and differentiation into antibody-secreting plasma cells or memory B cells. In autoimmune contexts such as SLE, these receptors facilitate the production of pathogenic anti-dsDNA antibodies that form immune complexes, contributing to tissue inflammation and organ damage. Several strategies have been explored for targeting dsDNA-specific BCR-expressing cells, including Chimeric Autoantibody Receptors and Peptide Blockers. Detection of circulating anti-dsDNA antibodies is a diagnostic criterion for SLE, and the presence of high-affinity IgG class-switched variants correlates strongly with disease activity.
Inhibition of B cell proliferation/activation
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