ArticleImmunology1999
Altered distribution of intraglomerular immune complexes in C3-deficient mice.
Article in Immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Characteristics of membranoproliferative glomerulonephritis based on a new classification at a single center.Clinical and experimental nephrology · 2019Article
- Complement in Lupus Nephritis: New Perspectives.Kidney diseases (Basel, Switzerland) · 2015Review
- Complement in glomerular injury.Seminars in immunopathology · 2007Review
- Experimental membranous nephropathy redux.American journal of physiology. Renal physiology · 2005Review
- Use of genetic knockouts to modulate disease expression in a murine model of lupus, MRL/lpr mice.Immunologic research · 2002Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have studied the role of complement in a model of glomerular inflammation induced by the in situ formation of immune complexes along the glomerular basement membrane. In C3-deficient mice, produced by homologous recombination, immune complex formation occurs initially in the subendothelial site and progresses slowly to the subepithelial position, whereas wild-type mice do not develop subendothelial deposits. In addition, the accumulation of electron-dense deposits is greater in the complement-deficient mice. Complement therefore influences glomerular handling of immune complexes, possibly because of changes in the physiochemical characteristics of the immune complexes. However, despite evidence of complement activation in the wild-type mice, as demonstrated by immunohistochemical detection of C3, C4 and C9, the degree of proteinuria was similar in C3-deficient mice. We conclude that, although complement is required for the normal glomerular metabolism of immune complexes, other, complement-independent, factors are involved in the generation of glomerular injury in this model.
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Registered trials
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