ArticleMolecular immunology2007
Complement in experimental autoimmune encephalomyelitis revisited: C3 is required for development of maximal disease.
Article in Molecular immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Coagulation Factors Fibrinogen, Thrombin, and Factor XII in Inflammatory Disorders-A Systematic Review.Frontiers in immunology · 2018Pooled it
- Methyl-CpG-Binding Protein 2 Emerges as a Central Player in Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorders.Cellular and molecular neurobiology · 2023Review
- Roles and regulation of microglia activity in multiple sclerosis: insights from animal models.Nature reviews. Neuroscience · 2023Review
- Overview of diet and autoimmune demyelinating optic neuritis: a narrative review.Immunometabolism (Cobham, Surrey) · 2023Review
- C3-dependent effector functions of complement.Immunological reviews · 2023Review
- Genetics behind Cerebral Disease with Ocular Comorbidity: Finding Parallels between the Brain and Eye Molecular Pathology.International journal of molecular sciences · 2022Review
- Thermoregulatory dynamics reveal sex-specific inflammatory responses to experimental autoimmune encephalomyelitis in mice: Implications for multiple sclerosis-induced fatigue in females.Brain, behavior, & immunity - health · 2022Article
- The validity of animal models to explore the pathogenic role of the complement system in multiple sclerosis: A review.Frontiers in molecular neuroscience · 2022Review
- Free complement and complement containing extracellular vesicles as potential biomarkers for neuroinflammatory and neurodegenerative disorders.Frontiers in immunology · 2022Review
- Divergent complement system activation in two clinically distinct murine models of multiple sclerosis.Frontiers in immunology · 2022Article
- Complement component 3 from astrocytes mediates retinal ganglion cell loss during neuroinflammation.Acta neuropathologica · 2021Article
- Molecular Examination of Differentially Expressed Genes in the Brains of Experimental Autoimmune Encephalomyelitis Mice Post Herceptin Treatment.Journal of inflammation research · 2021Article
- Ataxin-1 regulates B cell function and the severity of autoimmune experimental encephalomyelitis.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Gene Expression Analysis of Astrocyte and Microglia Endocannabinoid Signaling during Autoimmune Demyelination.Biomolecules · 2020Article
- Complement-dependent synapse loss and microgliosis in a mouse model of multiple sclerosis.Brain, behavior, and immunity · 2020Article
- Targeted Complement Inhibition at Synapses Prevents Microglial Synaptic Engulfment and Synapse Loss in Demyelinating Disease.Immunity · 2020Article
- Synaptic Elimination in Neurological Disorders.Current neuropharmacology · 2019Review
- Gut dysbiosis breaks immunological tolerance toward the central nervous system during young adulthood.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Complement activation and expression during chronic relapsing experimental autoimmune encephalomyelitis in the Biozzi ABH mouse.Clinical and experimental immunology · 2015Article
- Lipocalin-2 protein deficiency ameliorates experimental autoimmune encephalomyelitis: the pathogenic role of lipocalin-2 in the central nervous system and peripheral lymphoid tissues.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Complement per se has been shown to play an important role in demyelinating disease but controversy remains regarding the role of C3 in the development and progression of experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis. In this study, we used C3(-/-) mice to confirm previous findings that C3 is required for full development of EAE. Furthermore, C3(+/-) mice (with serum C3 levels 50% that of wild-type mice) developed EAE with a severity intermediate between wild-type and C3(-/-) mice. Importantly transfer of wild-type encephalitogenic T cells to C3(-/-) mice resulted in attenuated EAE. C3(-/-) mice with EAE had fewer CD4(+) and CD8(+) T cells in the CNS and 50% fewer of these cells produced IFN-gamma compared to wild-type mice. When treated with anti-CD3 antibody, CD4(+) T cells from wild-type and C3(-/-) mice had similar activation profiles as judged by IFN-gamma production and CD25 and CD69 expression, indicating there is no gross or intrinsic defect in T cells from C3(-/-) mice. T cells from primed C3(-/-) mice proliferated comparably to that of control T cells on re-stimulation with MOG peptide. Our results confirm a requirement for C3 for maximal development of EAE and suggest that receptors for C3-derived activation fragments might be a viable therapeutic target for prevention and treatment demyelinating disease.
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Registered trials
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