ArticleMolecular immunology2009
C3a receptor deficiency accelerates the onset of renal injury in the MRL/lpr mouse.
Article in Molecular immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 44 citations in OpenAlex.
- Systemic lupus erythematosus as the paradigm for understanding the complex immune relationships and therapeutic opportunities for targeting complement in autoimmune diseases.Immunobiology · 2025Review
- Complement anaphylatoxins: Potential therapeutic target for diabetic kidney disease.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Alternative complement pathway activation in thrombotic microangiopathy associated with lupus nephritis.Clinical rheumatology · 2021Article
- The Complement C3a and C3a Receptor Pathway in Kidney Diseases.Frontiers in immunology · 2020Review
- Distinct roles of the anaphylatoxin receptors C3aR, C5aR1 and C5aR2 in experimental meningococcal infections.Virulence · 2019Article
- Possible role of complement factor H in podocytes in clearing glomerular subendothelial immune complex deposits.Scientific reports · 2019Article
- Donor pretreatment with nebulized complement C3a receptor antagonist mitigates brain-death induced immunological injury post-lung transplant.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018Article
- Complement regulation and kidney diseases: recent knowledge of the double-edged roles of complement activation in nephrology.Clinical and experimental nephrology · 2018Review
- Article
- Targeting the complement cascade: novel treatments coming down the pike.Kidney international · 2016Review
- Complement in Lupus Nephritis: New Perspectives.Kidney diseases (Basel, Switzerland) · 2015Review
- C3a and C5a promote renal ischemia-reperfusion injury.Journal of the American Society of Nephrology : JASN · 2012Article
- Heat shock protein 90 inhibition by 17-DMAG lessens disease in the MRL/lpr mouse model of systemic lupus erythematosus.Cellular & molecular immunology · 2012Article
- Treatment targets in systemic lupus erythematosus: biology and clinical perspective.Arthritis research & therapy · 2012Review
- Genetic Deficiency of Complement Component 3 Does Not Alter Disease Progression in a Mouse Model of Huntington's Disease.Journal of Huntington's disease · 2012Article
- Complement factor H deficiency accelerates development of lupus nephritis.Journal of the American Society of Nephrology : JASN · 2011Article
- Mechanisms of tissue injury in lupus nephritis.Arthritis research & therapy · 2011Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The development and progression of systemic lupus erythematosus (SLE) is strongly associated with complement activation and deposition. The anaphylatoxin C3a is a product of complement activation with immunomodulatory properties, and the receptor for C3a (C3aR) is not only expressed by granulocytes and antigen presenting cell populations, but it is also strongly up-regulated in lupus prone mice with active nephritis. In order to characterize the role of the C3aR in inflammatory nephritis, we bred C3aR knock out mice onto the MRL/lpr genetic background (C3aR KO MRL). Compared to control MRL/lpr mice, C3aR KO MRL mice had elevated auto-antibody titers and an earlier onset of renal injury. At 8 weeks, renal expression of a wide range of chemokines and chemokine receptors was increased in C3aR KO MRL kidneys compared to controls. Only the expression of MCP-1 was significantly decreased in the C3aR KO MRL mice. The increased chemokine and chemokine receptor expression seen in the C3aR KO MRL mice was associated with a more rapid rise in serum creatinine and the acceleration of renal fibrosis. However, loss of the C3aR had little impact on long-term kidney injury and did not alter survival. These findings suggest that activation of the C3aR plays a protective, not pathologic, role in the early phase of inflammatory nephritis in the MRL/lpr model of SLE.
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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.