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Systemic lupus erythematosus (SLE) is an autoimmune disease where improperly cleared apoptotic cells and neutrophil extracellular traps (NETs) induce an autoimmune response. Complement is crucial to prevent SLE by tailoring immune responses and opsonizing dead cells but may also induce inflammation and tissue damage once the disease is initiated. Complement C1q binds to apoptotic cells and ensures
