Systemic lupus erythematosus (SLE) is a chronic, multisystem human autoimmune disease characterized by the differentiation of short-and long-lived plasma cells (PCs) that secrete pathogenic autoantibodies (1–3). These include autoantibodies specific for DNA involved in glomerulonephritis, autoantibodies to phospholipid 2-glycoprotein I in thrombosis, and anti-Ro autoantibodies in congenital heart block. The exact cause of SLE is unclear, but the emergence of the disease appears to depend on a combination of genetic susceptibility and environmental factors that initiate and/or contribute to pathogenic autoimmunity. Candidate initiating factors include ultraviolet light, cigarette smoking, and infections with bacteria and/or viruses that polyclonally activate B cells. More frequent or aggressive disease is associated with female sex, African American and African Caribbean origin, and restricted educational experience. Genetic susceptibility loci include genes affecting activation, proliferation, cytokine secretion/responsiveness, and apoptosis of the T and B cells involved in humoral immunity, as well as genes involved in presentation and clearance of apoptotic material and autoantigens by antigen-presenting cells (APCs) and phagocytes (4).