ArticleClinical and experimental immunology2004
Blockade of the C5a receptor fails to protect against experimental autoimmune encephalomyelitis in rats.
Article in Clinical and experimental immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 32 citations in OpenAlex.
- Action of the Terminal Complement Pathway on Cell Membranes.The Journal of membrane biology · 2025Review
- The validity of animal models to explore the pathogenic role of the complement system in multiple sclerosis: A review.Frontiers in molecular neuroscience · 2022Review
- The role of the complement system in Multiple Sclerosis: A review.Frontiers in immunology · 2022Review
- A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis.Nature immunology · 2019Article
- Systemic inhibition of the membrane attack complex impedes neuroinflammation in chronic relapsing experimental autoimmune encephalomyelitis.Acta neuropathologica communications · 2018Article
- Mast Cells are Important Modifiers of Autoimmune Disease: With so Much Evidence, Why is There Still Controversy?Frontiers in immunology · 2012Article
- Role and mechanism of action of complement in regulating T cell immunity.Molecular immunology · 2010Review
- The role of the complement system and the activation fragment C5a in the central nervous system.Neuromolecular medicine · 2010Article
- Systemic and local anti-C5 therapy reduces the disease severity in experimental autoimmune uveoretinitis.Clinical and experimental immunology · 2010Article
- Deletion of both the C3a and C5a receptors fails to protect against experimental autoimmune encephalomyelitis.Neuroscience letters · 2009Article
- Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Complement in multiple sclerosis: its role in disease and potential as a biomarker.Clinical and experimental immunology · 2009Review
- Complement C5 regulates the expression of insulin-like growth factor binding proteins in chronic experimental allergic encephalomyelitis.Journal of neuroimmunology · 2008Article
- Complement C3 and C4 expression in C1q sufficient and deficient mouse models of Alzheimer's disease.Journal of neurochemistry · 2008Article
- Complement in experimental autoimmune encephalomyelitis revisited: C3 is required for development of maximal disease.Molecular immunology · 2007Article
- Complement membrane attack is required for endplate damage and clinical disease in passive experimental myasthenia gravis in Lewis rats.Clinical and experimental immunology · 2006Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement activation contributes to inflammation and tissue damage in human demyelinating diseases and in rodent models of demyelination. Inhibitors of complement activation ameliorate disease in the rat model antibody-dependent experimental autoimmune encephalomyelitis and rats unable to generate the membrane attack complex of complement develop inflammation without demyelination. The role of the highly active chemotactic and anaphylactic complement-derived peptide C5a in driving inflammation and pathology in rodent models of demyelination has been little explored. Here we have used a small molecule C5a receptor antagonist, AcF-[OPdChaWR], to examine the effects of C5a receptor blockade in rat models of brain inflammation and demyelination. C5a receptor antagonist therapy completely blocked neutrophil response to C5a in vivo but had no effect on clinical disease or resultant pathology in either inflammatory or demyelinating rat models. We conclude that C5a is not required for disease induction or perpetuation in these strongly complement-dependent disease models.
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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.