ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Cutting edge: the membrane attack complex of complement is required for the development of murine experimental cerebral malaria.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. 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, 23 citations in OpenAlex.
- Mouse NOD/Shi and NSY/Hos strains infected with Plasmodium berghei ANKA are models for experimental cerebral malaria.Experimental animals · 2025Article
- 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
- Multiplexed quantitative proteomics provides mechanistic cues for malaria severity and complexity.Communications biology · 2020Article
- Desperately Seeking Therapies for Cerebral Malaria.Journal of immunology (Baltimore, Md. : 1950) · 2020Review
- Mouse NC/Jic strain provides novel insights into host genetic factors for malaria research.Experimental animals · 2019Review
- Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Complement C5-deficient mice are protected from seizures in experimental cerebral malaria.Epilepsia · 2014Article
- Deletion of C-reactive protein ameliorates experimental cerebral malaria?Transactions of the Royal Society of Tropical Medicine and Hygiene · 2014Article
- Functional roles for C5a and C5aR but not C5L2 in the pathogenesis of human and experimental cerebral malaria.Infection and immunity · 2014Article
- Potential efficacy of citicoline as adjunct therapy in treatment of cerebral malaria.Antimicrobial agents and chemotherapy · 2014Article
- Innate immunity and neuroinflammation.Mediators of inflammation · 2013Review
- Deletion of the complement phagocytic receptors CR3 and CR4 does not alter susceptibility to experimental cerebral malaria.Parasite immunology · 2012Article
- Pathogenesis of malaria revisited.Medical microbiology and immunology · 2012Review
- The C5 convertase is not required for activation of the terminal complement pathway in murine experimental cerebral malaria.The Journal of biological chemistry · 2012Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Cerebral malaria is the most severe complication of Plasmodium falciparum infection and accounts for a large number of malaria fatalities worldwide. Recent studies demonstrated that C5(-/-) mice are resistant to experimental cerebral malaria (ECM) and suggested that protection was due to loss of C5a-induced inflammation. Surprisingly, we observed that C5aR(-/-) mice were fully susceptible to disease, indicating that C5a is not required for ECM. C3aR(-/-) and C3aR(-/-) × C5aR(-/-) mice were equally susceptible to ECM as were wild-type mice, indicating that neither complement anaphylatoxin receptor is critical for ECM development. In contrast, C9 deposition in the brains of mice with ECM suggested an important role for the terminal complement pathway. Treatment with anti-C9 Ab significantly increased survival time and reduced mortality in ECM. Our data indicate that protection from ECM in C5(-/-) mice is mediated through inhibition of membrane attack complex formation and not through C5a-induced inflammation.
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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.