Genetic dissection of lupus nephritis in murine models of SLE

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with extremely heterogeneous clinical features, varying in pathogenicity from mild forms of the disease to those that advance relentlessly leading to progressive end organ damage. The underlying autoimmune disorder can express as a variety of immunologic abnormalities but generally results in the production of autoantibodies primarily directed against a spectrum of nuclear antigens. Much of the pathogenicity of SLE results from inflammatory processes initiated as a consequence of either the deposition of immune complexes or the targeting of autoantibodies to various anatomic sites. The most serious clinical consequences of SLE result from immune complex deposition in the kidney, resulting in lupus nephritis and culminating in kidney failure.