| First Author | Nakatsuru S | Year | 1999 |
| Journal | Pathol Int | Volume | 49 |
| Issue | 11 | Pages | 974-82 |
| PubMed ID | 10594844 | Mgi Jnum | J:78614 |
| Mgi Id | MGI:2385547 | Doi | 10.1046/j.1440-1827.1999.00979.x |
| Citation | Nakatsuru S, et al. (1999) Genetic dissection of the complex pathological manifestations of collagen disease in MRL/lpr mice. Pathol Int 49(11):974-82 |
| abstractText | An MRL strain of mice bearing a Fas-deletion mutant gene, lpr, MRL/MpJ-lpr/lpr (MRL/lpr) develops collagen disease involving vasculitis, glomerulonephritis, arthritis and sialoadenitis, each of which has been studied as a model for polyarteritis, lupus nephritis, rheumatoid arthritis and Sjogren's syndrome, respectively. Development of such lesions seems dependent on host genetic background since the congenic C3H/HeJ-lpr/lpr (C3H/lpr) mice rarely develop them. To identify the gene loci affecting each lesion, a genetic dissection of these complex pathological manifestations was carried out. First, histopathological features in MRL/lpr, C3H/lpr, (MRL/lpr x C3H/lpr) F1 intercross, and MRL/lpr x (MRL/lpr x C3H/lpr) F1 backcross mice were analyzed. Genomic DNA of the backcross mice were subjected to association studies by Chi-squared analysis for determining which polymorphic microsatellite locus occurs at higher frequency among affected compared to unaffected individuals for each lesion. As a result, gene loci recessively associated with each lesion were mapped on different chromosomal positions. We concluded that each of these lesions in MRL/lpr mice is under the control of a different set of genes, suggesting that the complex pathological manifestations of collagen disease result from polygenic inheritance. |
