ArticleThe American journal of pathology2006
Deficiency of C4 from donor or recipient mouse fails to prevent renal allograft rejection.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- Complement-targeted therapies in kidney transplantation-insights from preclinical studies.Frontiers in immunology · 2022Review
- Membrane attack complexes, endothelial cell activation, and direct allorecognition.Frontiers in immunology · 2022Review
- A potent truncated form of human soluble CR1 is protective in a mouse model of renal ischemia-reperfusion injury.Scientific reports · 2021Article
- Recent advances into the role of pattern recognition receptors in transplantation.Cellular immunology · 2020Review
- High-activity Classical and Alternative Complement Pathway Genotypes-Association With Donor-specific Antibody-triggered Injury and Renal Allograft Survival.Transplantation direct · 2020Article
- Ischemia and Reperfusion Injury in Kidney Transplantation: Relevant Mechanisms in Injury and Repair.Journal of clinical medicine · 2020Review
- Post-transplant Alternative Complement Pathway Activation Influences Kidney Allograft Function.Archivum immunologiae et therapiae experimentalis · 2019Article
- Complement Recognition Pathways in Renal Transplantation.Journal of the American Society of Nephrology : JASN · 2017Review
- Complement involvement in kidney diseases: From physiopathology to therapeutical targeting.World journal of nephrology · 2015Review
- Mouse kidney transplantation: models of allograft rejection.Journal of visualized experiments : JoVE · 2014Article
- Complement cascade and kidney transplantation: The rediscovery of an ancient enemy.World journal of transplantation · 2014Review
- The role of complement in the pathogenesis of renal ischemia-reperfusion injury and fibrosis.Fibrogenesis & tissue repair · 2014Review
- The role of the complement system in acute kidney injury.Seminars in nephrology · 2013Review
- The complement system in ischemia-reperfusion injuries.Immunobiology · 2012Review
- The lectin pathway of complement activation is a critical component of the innate immune response to pneumococcal infection.PLoS pathogens · 2012Article
- Which pathways trigger the role of complement in ischaemia/reperfusion injury?Frontiers in immunology · 2012Article
- Targeting of mannan-binding lectin-associated serine protease-2 confers protection from myocardial and gastrointestinal ischemia/reperfusion injury.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Genotypic diversity of complement component C4 does not predict kidney transplant outcome.Journal of the American Society of Nephrology : JASN · 2011Article
- Complement in organ transplantation.Current opinion in organ transplantation · 2010Review
- Complement gene expression in human cardiac allograft biopsies as a correlate of histologic grade of injury.Transplantation · 2008Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Complement effector products generated in the transplanted kidney are known to mediate transplant rejection, but which of the three main activation pathways of complement trigger this response is unclear. Here we assessed the role of the classical and lectin pathways by studying the common component C4 in mouse kidney transplant rejection. We transplanted wild-type or C4-null H-2(b) donor kidneys into H-2(k) or H-2(d) recipients, or vice-versa, to assess the roles of donor kidney and recipient expression of complement. Intragraft C4 gene expression rose substantially during rejection. However, we found no significant association between graft acceptance and the presence of C4 in either the donor kidney or recipient mouse. At the time of rejection, we found no significant differences in alloantibody response in the different groups. Tubular deposition of C3 to C9 occurred regardless of the absence or presence of C4 in either the donor or recipient mouse, indicating that C4 was dispensable for complement activation at this site. These data suggest that complement activation and renal allograft rejection are independent of the classical and lectin pathways in these models, implying that in the absence of these pathways the alternative pathway is the main trigger for complement-mediated rejection.
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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.