Interaction of mutant lpr gene with background strain influences renal disease.
The mutant gene lpr on the MRL/Mp strain of mice is responsible for converting a late onset glomerulonephritis into an early, aggressive, and fatal renal disease. This gene induces the proliferation of a unique subset of lymphocytes, the production of a variety of autoantibodies and shortened survival in MRL/Mp as well as in the genetically distinct strains C3H/HeJ, C57BL/6J, and AKR/J. The present study examined in detail the role of the lpr gene in the formation of lupus nephritis. The results show that C3H-lpr and B6-lpr mice do not develop nephritis while the AKR-lpr strain has a mild form of renal disease. None of these newly constructed congenic mutant strains have the severity of proteinuria or the degree of renal pathology characteristic of MRL-lpr mice. Thus, the lpr gene alone is insufficient in producing severe renal injury. The interaction of the lpr gene with other factors is required for the induction of life-threatening lupus nephritis.
D000818:Animals; D005260:Female; D005796:Genes; D005804:Genes, Lethal; D007678:Kidney Glomerulus / Q000276:immunology / Q000473:pathology; D008180:Lupus Erythematosus, Systemic / Q000209:etiology / Q000235:genetics; D008198:Lymph Nodes / Q000032:analysis; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics*; D009026:Mortality; D009154:Mutation; D009393:Nephritis / Q000209:etiology / Q000235:genetics; D009929:Organ Size; D011507:Proteinuria / Q000378:metabolism