| First Author | Xie C | Year | 2007 |
| Journal | Clin Immunol | Volume | 124 |
| Issue | 1 | Pages | 49-56 |
| PubMed ID | 17500042 | Mgi Jnum | J:123515 |
| Mgi Id | MGI:3718759 | Doi | 10.1016/j.clim.2007.04.002 |
| Citation | Xie C, et al. (2007) Enhanced susceptibility to immune nephritis in DBA/1 mice is contingent upon IL-1 expression. Clin Immunol 124(1):49-56 |
| abstractText | The DBA/1 mouse strain is particularly sensitive to experimental immune-mediated nephritis. Previous studies have indicated that various chemokines/cytokines are elevated in strains of mice susceptible to immune-mediated glomerulonephritis. One of the many elevated cytokines is IL-1. This study was designed to determine if IL-1 is essential for the development of immune-mediated nephritis in the DBA/1 mouse strain that is particularly sensitive to this disease. Both male and female DBA/1 mice and DBA/1.IL-1R1(-/-) mice were challenged with anti-GBM sera. We then compared DBA/1 mice to DBA/1.IL-1R1(-/-) mice to determine the influence of IL-1 on immune-mediated nephritis. Compared to DBA/1 mice, DBA/1.IL-1R1(-/-) mice excreted significantly less protein post anti-GBM serum challenge. None of the DBA/1.IL-1R1(-/-) mice, male or female, had a BUN higher than 22 mg/dl post-challenge whereas wild-type DBA/1 mice had significantly elevated BUN. Wild-type DBA/1 mice exhibited pronounced glomerulonephritis, with crescent formation, as well as tubulo-interstitial disease compared to DBA/1.IL1R1(-/-) mice. These findings indicate that IL-1 is necessary for the development of nephritis in DBA/1 mice and suggest that the elevated IL-1 levels in these mice may be one reason why the DBA/1 strain is particularly sensitive to multiple end organ diseases. |
