ArticleThe Journal of experimental medicine2008
C5 deficiency and C5a or C5aR blockade protects against cerebral malaria.
Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 102 citations in OpenAlex.
- A Targeted Blockade of Terminal C5a Is Critical to Management of Sepsis and Acute Respiratory Distress Syndrome: The Mechanism of Action of Vilobelimab.International journal of molecular sciences · 2025Review
- A whole blood assay for antibody dependent phagocytosis of Plasmodium falciparum infected erythrocytes.Communications medicine · 2025Article
- The Importance of Murine Models in Determining In Vivo Pharmacokinetics, Safety, and Efficacy in Antimalarial Drug Discovery.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Mouse NOD/Shi and NSY/Hos strains infected with Plasmodium berghei ANKA are models for experimental cerebral malaria.Experimental animals · 2025Article
- Innate Immune Mechanisms in the Central Nervous System.Advances in experimental medicine and biology · 2025Review
- A novel locus inFrontiers in genetics · 2024Article
- Pathogenetic mechanisms and treatment targets in cerebral malaria.Nature reviews. Neurology · 2023Review
- The Defensive Interactions of Prominent Infectious Protozoan Parasites: The Host's Complement System.Biomolecules · 2022Review
- Interaction Between the Complement System and Infectious Agents - A Potential Mechanistic Link to Neurodegeneration and Dementia.Frontiers in cellular neuroscience · 2021Review
- Beyond Binding: The Outcomes of Antibody-Dependent Complement Activation in Human Malaria.Frontiers in immunology · 2021Review
- Pathophysiology and neurologic sequelae of cerebral malaria.Malaria journal · 2020Review
- Desperately Seeking Therapies for Cerebral Malaria.Journal of immunology (Baltimore, Md. : 1950) · 2020Review
- New insights into microvascular injury to inform enhanced diagnostics and therapeutics for severe malaria.Virulence · 2019Review
- Aptamer-Conjugated Framework Nucleic Acids for the Repair of Cerebral Ischemia-Reperfusion Injury.Nano letters · 2019Article
- Mouse NC/Jic strain provides novel insights into host genetic factors for malaria research.Experimental animals · 2019Review
- Cytokine Profile in Early Infection byJournal of immunology research · 2019Article
- Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Blockade of the C5a-C5aR axis alleviates lung damage in hDPP4-transgenic mice infected with MERS-CoV.Emerging microbes & infections · 2018Article
- TCRβ-expressing macrophages induced by a pathogenic murine malaria correlate with parasite burden and enhanced phagocytic activity.PloS one · 2018Article
- A Plasmodium yoelii HECT-like E3 ubiquitin ligase regulates parasite growth and virulence.Nature communications · 2017Article
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Experimental infection of mice with Plasmodium berghei ANKA (PbA) provides a powerful model to define genetic determinants that regulate the development of cerebral malaria (CM). Based on the hypothesis that excessive activation of the complement system may confer susceptibility to CM, we investigated the role of C5/C5a in the development of CM. We show a spectrum of susceptibility to PbA in a panel of inbred mice; all CM-susceptible mice examined were found to be C5 sufficient, whereas all C5-deficient strains were resistant to CM. Transfer of the C5-defective allele from an A/J (CM resistant) onto a C57BL/6 (CM-susceptible) genetic background in a congenic strain conferred increased resistance to CM; conversely, transfer of the C5-sufficient allele from the C57BL/6 onto the A/J background recapitulated the CM-susceptible phenotype. The role of C5 was further explored in B10.D2 mice, which are identical for all loci other than C5. C5-deficient B10.D2 mice were protected from CM, whereas C5-sufficient B10.D2 mice were susceptible. Antibody blockade of C5a or C5a receptor (C5aR) rescued susceptible mice from CM. In vitro studies showed that C5a-potentiated cytokine secretion induced by the malaria product P. falciparum glycosylphosphatidylinositol and C5aR blockade abrogated these amplified responses. These data provide evidence implicating C5/C5a in the pathogenesis of CM.
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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.