Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the appearance of autoantibodies against a variety of nucleosomal and kidney antigens. Targeting of glomeruli, the basic units of filtration in the kidneys, by these autoantibodies is one of the crucial events initiating nephritis, leading to the chronic renal insufficiency seen in lupus. Here we review published reports that directly tested the in vivo pathogenicity of antinuclear/glomerular autoantibodies, which indicate that intermediating nucleosomal bridges might be what empower antibodies to target glomeruli. Further studies that systematically evaluate the contribution of clearly non-DNA binding nephritogenic antibodies, and elucidate the additional factors essential for renal pathology to ensue once the golmeruli are targeted, remain to be done.
Limaye, N., & Mohan, C. (2004). Pathogenicity of anti-DNA/glomerular autoantibodies – weighing the evidence. Drug Discovery Today: Disease Models, 1(4), 395-403. https://doi.org/10.1016/j.ddmod.2004.11.008 (Original work published 2004)