| First Author | Kelley VE | Year | 1985 |
| Journal | Clin Immunol Immunopathol | Volume | 37 |
| Issue | 2 | Pages | 220-9 |
| PubMed ID | 4042431 | Mgi Jnum | J:109439 |
| Mgi Id | MGI:3628960 | Doi | 10.1016/0090-1229(85)90153-9 |
| Citation | Kelley VE, et al. (1985) Interaction of mutant lpr gene with background strain influences renal disease. Clin Immunol Immunopathol 37(2):220-9 |
| abstractText | 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. |
