Abstract
Systemic lupus erythematosus (SLE) is a B-cell–dependent autoimmune disease that is characterized by autoantibodies specific for nuclear antigens such as dsDNA and histones. Apoptotic blebs released from dying cells are thought to represent a major source of autoantigen. The cellular and molecular basis for SLE is not known but a major risk factor is deficiency in products of natural immunity. For example, individuals deficient in serum complement proteins C1q or C4 almost always develop lupus1. This presents a paradox as the complement system is known to mediate pathogenesis in SLE. In addition to its known role in inflammation, the complement system participates in humoral antibody responses via enhancement of B-lymphocyte activation, germinal center survival and maintenance of long-term effector responses2.
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