Logo of clinexpimmunolLink to Publisher's site
Clin Exp Immunol. Dec 1997; 110(3): 403–409.
PMCID: PMC1904827

Protection against anti-glomerular basement membrane (GBM)-mediated nephritis in C3- and C4-deficient mice


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/24 h, 0.059 mg/24 h and 0.327 ± 0.14 mg/24 h 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.

Keywords: complement, deficiency, knockout mice, anti-glomerular basement membrane disease, glomerulonephritis

Full Text

The Full Text of this article is available as a PDF (784K).

Articles from Clinical and Experimental Immunology are provided here courtesy of British Society for Immunology


Related citations in PubMed

See reviews...See all...

Cited by other articles in PMC

See all...


Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...