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REVIEW article
Front. Immunol.
Sec. Multiple Sclerosis and Neuroimmunology
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1530977
This article is part of the Research TopicMonoclonal antibodies in treating multiple sclerosis (MS), and related diseases.View all 11 articles
Translational Insights from EAE Models：Decoding MOGAD Pathogenesis and Therapeutic Innovation
Provisionally accepted
Yanjia Zhang1,2
Dong Li1*- 1Tianjin Children's Hospital, Tianjin, China
- 2Medicine, Tianjin University, Tianjin, Tianjin, China
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Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) is a rare acquired demyelinating syndrome manifesting as optic neuritis (ON), transverse myelitis (TM), acute disseminated encephalomyelitis (ADEM), and brainstem encephalitis. The disease is characterized by serum autoantibodies targeting myelin oligodendrocyte glycoprotein (MOG), which is exclusively expressed on central nervous system (CNS) myelin and oligodendrocyte membranes. Experimental autoimmune encephalomyelitis (EAE) models have been instrumental in elucidating how these antibodies trigger complement-dependent cytotoxicity (CDC) and antibody-dependent cellular responses, leading to inflammatory demyelination. With most patients experiencing relapses and approximately 50% developing permanent disabilities, therapeutic strategies focus on reducing relapse frequency and severity. MOG-EAE models have directly informed acute treatment approaches including corticosteroids, plasma exchange (PLEX), and intravenous immunoglobulin (IVIG). Mechanistic studies in MOG-EAE models have revealed complex treatment responses and identified several translational targets, including complement inhibition, B-cell depletion strategies, and cytokine-directed therapies that are now advancing to clinical trials.. Current immunosuppressive therapies include azathioprine (AZA), mycophenolate mofetil (MMF), and rituximab (RTX), with their differential efficacy in MOGAD versus MS and AQP4-NMOSD now explained by EAE model findings on distinct immunopathological mechanisms. Guided by EAE translational insights into MOGAD pathophysiology, ongoing clinical trials are evaluating novel targeted therapies including complement inhibitors, plasma cell-depleting agents, and antigen-specific tolerization approaches.These EAE-derived mechanistic insights are critical for developing personalized treatment strategies that address the unique immunopathology of this challenging condition.
Keywords: Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disorder (MOGAD), Experimental autoimmune encephalomyelitis (EAE), pathophysiology, innate immunity, Adaptive Immunity, treatment strategies
Received: 19 Nov 2024; Accepted: 21 Apr 2025.
Copyright: © 2025 Zhang and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dong Li, Tianjin Children's Hospital, Tianjin, China
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