ReviewFrontiers in molecular neuroscience2022
The validity of animal models to explore the pathogenic role of the complement system in multiple sclerosis: A review.
Review in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Exosomes as mediators of repair and immunoregulation in multiple sclerosis: a new frontier in cell-free therapy.Molecular biology reports · 2026Review
- Broad-spectrum antiviral brincidofovir inhibits Epstein-Barr virus and related gammaherpesvirus in human and nonhuman primate cells.The Journal of clinical investigation · 2026Article
- Pidotimod alleviated experimental autoimmune encephalomyelitis by regulating the balance of splenic lymphocytes.BMC immunology · 2025Article
- Dissection of Neurotropic Theiler's Murine Encephalomyelitis Virus Induced Brain Atrophy in Single MHC Class I Mice of C57BL/6 Background.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Proteomic analysis reveals candidate molecules to mediate cortical pathology and identify possible biomarkers in an animal model of multiple sclerosis.Frontiers in immunology · 2025Article
- Association of Complement Factors With Disability Progression in Primary Progressive Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- Attenuation of ventriculomegaly and iron overload after intraventricular hemorrhage by membrane attack complex inhibition.Journal of neurosurgery · 2024Article
- The complement system in neurodegenerative and inflammatory diseases of the central nervous system.Frontiers in neurology · 2024Review
- Mice deficient in complement C3 are protected against recognition memory deficits and astrogliosis induced by status epilepticus.Frontiers in molecular neuroscience · 2023Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Animal models of multiple sclerosis (MS) have been extensively used to characterize the disease mechanisms in MS, as well as to identify potential pharmacologic targets for this condition. In recent years, the immune complement system has gained increased attention as an important effector in the pathogenesis of MS. Evidence from histological, serum, and CSF studies of patients supports an involvement of complement in both relapsing-remitting and progressive MS. In this review, we discuss the history and advances made on the use of MS animal models to profile the effects of the complement system in this condition. The first studies that explored the complement system in the context of MS used cobra venom factor (CVF) as a complement depleting agent in experimental autoimmune encephalomyelitis (EAE) Lewis rats. Since then, multiple mice and rat models of MS have revealed a role of C3 and the alternative complement cascade in the opsonization and phagocytosis of myelin by microglia and myeloid cells. Studies using viral vectors, genetic knockouts and pharmacologic complement inhibitors have also shown an effect of complement in synaptic loss. Antibody-mediated EAE models have revealed an involvement of the C1 complex and the classical complement as an effector of the humoral response in this disease. C1q itself may also be involved in modulating microglia activation and oligodendrocyte differentiation in these animals. In addition, animal and
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