| First Author | Sheerin NS | Year | 1997 |
| Journal | Clin Exp Immunol | Volume | 110 |
| Issue | 3 | Pages | 403-9 |
| PubMed ID | 9409643 | Mgi Jnum | J:44715 |
| Mgi Id | MGI:1101229 | Doi | 10.1046/j.1365-2249.1997.4261438.x |
| Citation | Sheerin NS, et al. (1997) Protection against anti-glomerular basement membrane (GBM)-mediated nephritis in C3- and C4-deficient mice. Clin Exp Immunol 110(3):403-9 |
| abstractText | Mice rendered completely deficient of the complement components C3 or C4 were used to determine the influence of complement activation in the heterologous phase of the anti-GBM disease model. In wild-type animals the disease is characterized by a neutrophil infiltrate, capillary thrombosis, proteinuria and C3 and C4 deposited within the glomerulus. The early infiltration of neutrophils into the glomeruli is greater in wild-type mice (2.8 +/- 0.3) compared with C3-deficient (1.4 +/- 0.2) and C4-deficient (1.2 +/- 0.003) mice. Deficiency also protects against the subsequent development of proteinuria (2.99 +/- 1.11 mg/24h, 0.059 mg/24h and 0.327 +/- 0.14 mg/24h in wild-type, C3-deficient and C4-deficient mice, respectively) and decreases glomerular capillary thrombosis in both C3- and C4-deficient mice. The degree of protection is greater in the C3-deficient than the C4-deficient animals, suggesting both classical and alternative pathway involvement. These studies support a critical role for complement in the development of anti-GBM disease. However, the protective effect of complement deficiency can be broken if the dose of nephritogenic antibody is increased. |
