| First Author | Bao L | Year | 2007 |
| Journal | Lab Invest | Volume | 87 |
| Issue | 4 | Pages | 357-64 |
| PubMed ID | 17259999 | Mgi Jnum | J:141594 |
| Mgi Id | MGI:3818829 | Doi | 10.1038/labinvest.3700522 |
| Citation | Bao L, et al. (2007) Decay-accelerating factor but not CD59 limits experimental immune-complex glomerulonephritis. Lab Invest 87(4):357-64 |
| abstractText | The complex balance between the pro-activating and regulatory influences of the complement system can affect the pathogenesis of immune complex-mediated glomerulonephritis (ICGN). Key complement regulatory proteins include decay accelerating factor (DAF) and CD59, which inhibit C3 activation and C5b-9 generation, respectively. Both are glycosylphosphatidylinositol-linked cell membrane proteins, which are widely distributed in humans and mice. Chronic serum sickness induced by daily immunization with horse spleen apoferritin over 6 weeks was used to induce ICGN in DAF-, CD59- and DAF/CD59-deficient mice, with wild-type littermate mice serving as controls. Both DAF and DAF/CD59-deficient mice had an increased incidence of GN relative to wild-type controls associated with significantly increased glomerular C3 deposition. Disease expression in CD59-deficient mice was no different than wild-type controls. DAF- and DAF/CD59-deficient mice also had increased monocyte chemoattractant protein-1 mRNA expression and glomerular infiltration with CD45(+) leukocytes. Our findings suggest that activation of C3 is strongly associated with experimental ICGN while downstream formation of C5b-9 is of lesser pathogenic importance in this model. |
