Mediators of injury in lupus nephritis

Curr Opin Rheumatol. 2002 Sep;14(5):498-503. doi: 10.1097/00002281-200209000-00003.


Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by the production of autoantibodies and the development of immune complex glomerulonephritis. Lupus nephritis (LN) remains a leading cause of morbidity and mortality in SLE. As a result, defining pathogenetic mediators in LN remains a major research effort. Progression to LN in SLE is dependent on the host breaking immune tolerance and forming autoantibodies that deposit in the kidney. A variety of predisposing factors in the host must then be present for this event to result in renal pathology. In this article, the authors review recent reports that advance our understanding of LN disease mediators, from autoantibody production and immune complex deposition to end stage fibrosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Antigen-Antibody Complex / immunology
  • Autoantibodies / immunology
  • Fibrosis / immunology
  • Fibrosis / pathology
  • Humans
  • Inflammation Mediators / immunology*
  • Lupus Nephritis / immunology*
  • Lupus Nephritis / pathology


  • Antigen-Antibody Complex
  • Autoantibodies
  • Inflammation Mediators