Abstract
Systemic lupus erythematosus is a generalized autoimmune disease affecting multiple end-organs including the kidneys. Glomerulonephritis is a leading cause of death in lupus, both in patients and murine models that develop disease spontaneously. Genetic mapping studies have uncovered several genetic intervals that confer susceptibility to nephritis both in human beings and in mice. This review surveys the genomic positions of these nephritis susceptibility loci in murine lupus. Currently we know very little about the molecular identities of the culprit genes within these mapped loci and whether these genetic elements contribute to nephritis directly in a renal-intrinsic fashion or indirectly by augmenting the formation of pathogenic autoantibodies. The next decade is likely to witness a significant broadening of our understanding of how different genes and molecules might facilitate end-organ damage in lupus.
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