Interaction of mutant lpr gene with background strain influences renal disease

Clin Immunol Immunopathol. 1985 Nov;37(2):220-9. doi: 10.1016/0090-1229(85)90153-9.


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.

Publication types

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

MeSH terms

  • Animals
  • Female
  • Genes
  • Genes, Lethal
  • Kidney Glomerulus / immunology
  • Kidney Glomerulus / pathology
  • Lupus Erythematosus, Systemic / etiology
  • Lupus Erythematosus, Systemic / genetics
  • Lymph Nodes / analysis
  • Mice
  • Mice, Inbred Strains / genetics*
  • Mortality
  • Mutation
  • Nephritis / etiology
  • Nephritis / genetics
  • Organ Size
  • Proteinuria / metabolism