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Although the exact etiology of systemic lupus erythematosus (SLE) remains elusive, B‐cell hyperactivity and production of autoantibodies directed to components of the cell nucleus are a well‐established pathogenetic mechanism of the disease. Therefore, the targeted inhibition of DNA‐specific B cells is a logical therapeutic approach. The complement receptor type 1 (CR1, CD35) has been shown to suppress...
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