ArticleKidney international2012
The C5a receptor has a key role in immune complex glomerulonephritis in complement factor H-deficient mice.
Article in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Androgens contribute to sex bias of autoimmunity in mice by T cell-intrinsic regulation of Ptpn22 phosphatase expression.Nature communications · 2024Article
- Cardiotrophin-1 therapy reduces disease severity in a murine model of glomerular disease.Physiological reports · 2024Article
- Macrophage Depletion Reduces Disease Pathology in Factor H-Dependent Immune Complex-Mediated Glomerulonephritis.Journal of immunology research · 2022Article
- The varying roles of macrophages in kidney injury and repair.Current opinion in nephrology and hypertension · 2020Review
- Macrophages: versatile players in renal inflammation and fibrosis.Nature reviews. Nephrology · 2019Review
- Muscle, myeloid cells, and complement: a complex interaction.Cellular & molecular immunology · 2018Article
- Getting over our Immune-Complex - C5a receptor blockade is the answer.Cellular & molecular immunology · 2017Article
- Abrogation of immune complex glomerulonephritis by native carboxypeptidase and pharmacological antagonism of the C5a receptor.Cellular & molecular immunology · 2016Article
- C5a Induces the Synthesis of IL-6 and TNF-α in Rat Glomerular Mesangial Cells through MAPK Signaling Pathways.PloS one · 2016Article
- CD11b is protective in complement-mediated immune complex glomerulonephritis.Kidney international · 2015Article
- Article
- Complement regulation in renal disease models.Seminars in nephrology · 2013Review
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4 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic serum sickness leads to the formation of glomerular immune complexes; however, C57BL/6 mice do not develop glomerulonephritis unless complement factor H (CFH) is absent from the plasma. Here we studied the role for C5a receptor (R) in this setting. The exaggerated humoral immune response in CFH(-/-) mice was normalized in CFH(-/-)C5aR(-/-) double knockout mice, highlighting the C5aR dependence. The CFH knockout mice developed proliferative glomerulonephritis with endocapillary F4/80+ macrophage infiltration, a process reduced in the double knockout mice. There was no interstitial inflammation by histologic criteria or flow cytometry for F4/80+ Ly6C(hi)CCR2(hi) inflammatory macrophages. There were, however, more interstitial CD3+ CD4+ T lymphocytes in CFH knockout mice with chronic serum sickness, while double knockout mice had greater than 5-fold more Ly6C(lo)CCR2(lo) anti-inflammatory macrophages compared to the CFH knockout mice. Mice lacking C5aR were significantly protected from functional renal disease as assessed by blood urea nitrogen levels. Thus, IgG- and iC3b-containing immune complexes are not inflammatory in C57BL/6 mice. Yet when these mice lack CFH, sufficient C3b persists in glomeruli to generate C5a and activate C5aR.
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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.