Abstract
Systemic lupus erythematosus (SLE) is the prototypic autoimmune disease, characterized by autoantibody production and immune complex (IC) deposition in tissues. A central facet of the pathophysiology of lupus involves defective clearance mechanisms. Defects in the clearance of apoptotic cells (ACs) and cellular debris may be responsible for initiating the loss of self-tolerance and development of systemic autoimmunity in SLE. Autoantigens are released from secondary necrotic cells and from NETosis, a form of cell death in which neutrophils extrude DNA and other nuclear and cytoplasmic material from the cell, with defective degradation of resulting DNA-containing neutrophil extracellular traps (NETs). Defective clearance of autoantibody-autoantigen IC by leukocytes leads to inflammatory signaling, precipitating organ damage and cell death, which propagates the autoimmune response.
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