ArticleImmunology2009
Mesangial cell complement receptor 1-related protein y limits complement-dependent neutrophil accumulation in immune complex glomerulonephritis.
Article in Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Neutrophils and NETs in kidney disease.Nature reviews. Nephrology · 2025Review
- Complement regulation in renal disease models.Seminars in nephrology · 2013Review
- Complement factor H deficiency accelerates development of lupus nephritis.Journal of the American Society of Nephrology : JASN · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The absence of complement receptor 1 (CR1) related gene/protein y (Crry) leads to embryonic lethality as a result of unrestricted complement activation and concomitant neutrophil infiltration. Here we used Crry(-/-)C3(+/-) mice to investigate the role of Crry in the pathogenesis of immune complex glomerulonephritis (GN). After 3 weeks of immunization with horse spleen apoferritin, six of nine Crry(-/-) C3(+/-) mice and none of the six control C3(+/-) mice developed proliferative GN (P = 0.010). After 5 weeks of immunization, GN scores in Crry(-/-) C3(+/-) mice were 0.67 +/- 0.22 mean +/- standard error of the mean (SEM), compared with 0.32 +/- 0.16 in C3(+/-) mice. Glomerular hypercellularity was attributable to neutrophil infiltration in mice with GN (1.7 +/- 0.3/glomerulus) compared with those without GN (0.4 +/- 0.1/glomerulus) (P = 0.001). Absent staining for alpha-smooth muscle actin and proliferating cell nuclear antigen suggested that mesangial cell proliferation did not play a significant role in this model. Serum C3 levels in Crry(-/-) C3(+/-) mice were approximately 20% and 30% those of wild-type mice and C3(+/-) mice, respectively. To determine whether this acquired hypocomplementaemia was relevant to this GN model system, Crry(-/-) C3(+/-) mouse kidneys were transplanted into wild-type mice followed by immunization with apoferritin for 1 or 2 weeks. Surprisingly, none of the Crry(-/-) C3(+/-) mouse kidneys developed GN at these early time-points, indicating that increasing circulating C3 levels several-fold did not increase susceptibility to GN. Renal expression of decay-accelerating factor was not different among any of the groups studied. Thus, our data indicate that mesangial cell Crry limits complement activation and subsequent neutrophil recruitment in the setting of local immune complex deposition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.