ArticleThe Journal of clinical investigation2006
Myelin oligodendrocyte glycoprotein-specific T and B cells cooperate to induce a Devic-like disease in mice.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers.
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Who cites it
163 citing papers in PubMed, 333 citations in OpenAlex.
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- Mapping the Evolution of Experimental Autoimmune Encephalomyelitis Research (2000-2024): A Global Bibliometric and Knowledge Domain Analysis.Molecular neurobiology · 2026Review
- Anti-MOG IgG in EAE models clinical aspects of pediatric MOGAD.Frontiers in immunology · 2026Article
- ATG5 controls CD80 expression in B cells and shapes cognate CD4Autophagy · 2025Article
- AhR signaling in skin-resident CD207Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Integrin CD103 reveals a distinct developmental pathway of autoreactive thymocytes in TCR transgenic mice.Nature communications · 2025Article
- Follicle on the Roof: Tertiary Lymphoid Structures in Central Nervous System Autoimmunity.Immunological reviews · 2025Review
- CD4-Positive T-Cell Responses to MOG Peptides in MOG Antibody-Associated Disease.International journal of molecular sciences · 2025Article
- NLRX1 limits inflammatory neurodegeneration in the anterior visual pathway.Journal of neuroinflammation · 2025Article
- Cellular and Immunological Analysis of 2D2/Th Hybrid Mice Prone to Experimental Autoimmune Encephalomyelitis in Comparison with 2D2 and Th Lines.International journal of molecular sciences · 2024Article
- MOG CNS Autoimmunity and MOGAD.Neurology(R) neuroimmunology & neuroinflammation · 2024Review
- Single-Cell Profiling Indicates a Proinflammatory Role of Meningeal Ectopic Lymphoid Tissue in Experimental Autoimmune Encephalomyelitis.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- Single-cell profiling indicates a high similarity between immune cells in the cerebrospinal fluid and in meningeal ectopic lymphoid tissue in experimental autoimmune encephalomyelitis.Frontiers in immunology · 2024Article
- Complete Freund's adjuvant as a confounding factor in multiple sclerosis research.Frontiers in immunology · 2024Review
- A B cell-driven EAE mouse model reveals the impact of B cell-derived cytokines on CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Pathogenesis, Clinical Features, and Treatment of Patients with Myelin Oligodendrocyte Glycoprotein (MOG) Autoantibody-Associated Disorders Focusing on Optic Neuritis with Consideration of Autoantibody-Binding Sites: A Review.International journal of molecular sciences · 2023Review
- T cell deletional tolerance restricts AQP4 but not MOG CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
103 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
Multiple sclerosis (MS) is a clinically and pathologically heterogeneous inflammatory/demyelinating disease of the CNS. In the MS variant Devic disease, lesions are predominantly found in the optic nerves and spinal cord but not the brain. The immunological bases of the different forms of MS are unknown. We previously generated myelin oligodendrocyte glycoprotein-specific (MOG-specific) TCR transgenic mice (TCRMOG mice; also referred to as 2D2 mice) and reported that a large proportion of these mice develop spontaneous isolated optic neuritis. We have now crossed the TCRMOG mice with MOG-specific Ig heavy-chain knock-in mice (IgHMOG mice; also referred to as Th mice), in which one-third of the B cells are specific for MOG. In these mice, MOG-specific B cells are very efficient in presenting MOG to the transgenic T cells and undergo class switching to IgG1 in the presence of the transgenic T cells. Sixty percent of TCRMOG x IgHMOG mice spontaneously developed a severe form of experimental autoimmune encephalomyelitis (EAE). Histological examination of the CNS revealed a selective distribution of meningeal and parenchymal inflammatory lesions in the spinal cord and optic nerves. Thus, CNS antigen-specific T and B cells cooperate to induce a distinct clinicopathologic EAE pattern that closely replicates human Devic disease.
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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.