ArticleThe Journal of clinical investigation2003
Myelin/oligodendrocyte glycoprotein-deficient (MOG-deficient) mice reveal lack of immune tolerance to MOG in wild-type mice.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 144 citations in OpenAlex.
- Integrin CD103 reveals a distinct developmental pathway of autoreactive thymocytes in TCR transgenic mice.Nature communications · 2025Article
- Morphology of Oligodendroglial Cells.Advances in neurobiology · 2025Review
- Thymic self-antigen expression for immune tolerance and surveillance.Inflammation and regeneration · 2022Review
- Tbx1, a gene encoded in 22q11.2 copy number variant, is a link between alterations in fimbria myelination and cognitive speed in mice.Molecular psychiatry · 2022Article
- Use of CRISPR/Cas9-mediated disruption of CNS cell type genes to profile transduction of AAV by neonatal intracerebroventricular delivery in mice.Gene therapy · 2021Article
- Clinical characteristics of MOG antibody disease: two case reports.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Article
- Murine Esophagus Expresses Glial-Derived Central Nervous System Antigens.International journal of molecular sciences · 2021Article
- Progressive Retinal and Optic Nerve Damage in a Mouse Model of Spontaneous Opticospinal Encephalomyelitis.Frontiers in immunology · 2021Article
- The Integrated UPR and ERAD in Oligodendrocytes Maintain Myelin Thickness in Adults by Regulating Myelin Protein Translation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Alterations of peripheral nerve excitability in an experimental autoimmune encephalomyelitis mouse model for multiple sclerosis.Journal of neuroinflammation · 2020Article
- Comparative Analysis of T-Cell Responses to Aquaporin-4 and Myelin Oligodendrocyte Glycoprotein in Inflammatory Demyelinating Central Nervous System Diseases.Frontiers in immunology · 2020Article
- Proteomics of the corpus callosum to identify novel factors involved in hypomyelinated Niemann-Pick Type C disease mice.Molecular brain · 2019Article
- Myelin oligodendrocyte glycoprotein antibodies in neurological disease.Nature reviews. Neurology · 2019Review
- Experimental autoimmune encephalomyelitis in the common marmoset: a translationally relevant model for the cause and course of multiple sclerosis.Primate biology · 2019Review
- A new technology for increasing therapeutic protein levels in the brain over extended periods.PloS one · 2019Article
- Experimental Autoimmune Encephalomyelitis (EAE) as Animal Models of Multiple Sclerosis (MS).Cold Spring Harbor perspectives in medicine · 2018Review
- Antigen-Specificity in the Thymic Development and Peripheral Activity of CD4Frontiers in immunology · 2018Review
- Deletional tolerance prevents AQP4-directed autoimmunity in mice.European journal of immunology · 2017Article
- Distinct inflammatory phenotypes of microglia and monocyte-derived macrophages in Alzheimer's disease models: effects of aging and amyloid pathology.Aging cell · 2017Article
- Epitope-Specific Tolerance Modes Differentially Specify Susceptibility to Proteolipid Protein-Induced Experimental Autoimmune Encephalomyelitis.Frontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We studied the immunological basis for the very potent encephalitogenicity of myelin/oligodendrocyte glycoprotein (MOG), a minor component of myelin in the CNS that is widely used to induce experimental autoimmune encephalomyelitis (EAE). For this purpose, we generated a mutant mouse lacking a functional mog gene. This MOG-deficient mouse presents no clinical or histological abnormalities, permitting us to directly assess the role of MOG as a target autoantigen in EAE. In contrast to WT mice, which developed severe EAE following immunization with whole myelin, MOG-deficient mice had a mild phenotype, demonstrating that the anti-MOG response is a major pathogenic component of the autoimmune response directed against myelin. Moreover, while MOG transcripts are expressed in lymphoid organs in minute amounts, both MOG-deficient and WT mice show similar T and B cell responses against the extracellular domain of MOG, including the immunodominant MOG 35-55 T cell epitope. Furthermore, no differences in the fine specificity of the T cell responses to overlapping peptides covering the complete mouse MOG sequence were observed between MOG+/+ and MOG-/- mice. In addition, upon adoptive transfer, MOG-specific T cells from WT mice and those from MOG-deficient mice are equally pathogenic. This total lack of immune tolerance to MOG in WT C57BL/6 mice may be responsible for the high pathogenicity of the anti-MOG immune response as well as the high susceptibility of most animal strains to MOG-induced EAE.
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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.