ArticleThe Journal of biological chemistry2012
The C5 convertase is not required for activation of the terminal complement pathway in murine experimental cerebral malaria.
Article in The Journal of biological chemistry, 2012. 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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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Host complement C3 promotes malaria transmission by killing symbiotic bacteria in the mosquito midgut.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mouse NOD/Shi and NSY/Hos strains infected with Plasmodium berghei ANKA are models for experimental cerebral malaria.Experimental animals · 2025Article
- Article
- Protein therapeutics and their lessons: Expect the unexpected when inhibiting the multi-protein cascade of the complement system.Immunological reviews · 2023Review
- Interaction Between the Complement System and Infectious Agents - A Potential Mechanistic Link to Neurodegeneration and Dementia.Frontiers in cellular neuroscience · 2021Review
- 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 Protein C3 Suppresses Axon Growth and Promotes Neuron Loss.Scientific reports · 2017Article
- Complement and Antibody-mediated Enhancement of Red Blood Cell Invasion and Growth of Malaria Parasites.EBioMedicine · 2016Article
- Host immune responses to experimental infection of Plasmodium relictum (lineage SGS1) in domestic canaries (Serinus canaria).Parasitology research · 2015Article
- Complement C5-deficient mice are protected from seizures in experimental cerebral malaria.Epilepsia · 2014Article
- Lack of long-lasting hydrosalpinx in A/J mice correlates with rapid but transient chlamydial ascension and neutrophil recruitment in the oviduct following intravaginal inoculation with Chlamydia muridarum.Infection and immunity · 2014Article
- Article
- Functional roles for C5a and C5aR but not C5L2 in the pathogenesis of human and experimental cerebral malaria.Infection and immunity · 2014Article
- Article
- Experimental cerebral malaria develops independently of endothelial expression of intercellular adhesion molecule-1 (icam-1).The Journal of biological chemistry · 2013Article
- Intrathecal activation as a typical immune response within the central nervous system in angiostrongyliasis.The American journal of tropical medicine and hygiene · 2013Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Cerebral malaria (CM) is the most severe manifestation of clinical malaria syndromes and has a high fatality rate especially in the developing world. Recent studies demonstrated that C5(-/-) mice are resistant to experimental CM (ECM) and that protection was due to the inability to form the membrane attack complex. Unexpectedly, we observed that C4(-/-) and factor B(-/-) mice were fully susceptible to disease, indicating that activation of the classical or alternative pathways is not required for ECM. C3(-/-) mice were also susceptible to ECM, indicating that the canonical C5 convertases are not required for ECM development and progression. Abrogation of ECM by treatment with anti-C9 antibody and detection of C5a in serum of C3(-/-) mice confirmed that C5 activation occurs in ECM independent of C5 convertases. Our data indicate that activation of C5 in ECM likely occurs via coagulation enzymes of the extrinsic protease pathway.
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Registered trials
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