ReviewTherapeutic advances in neurological disorders2025
Induction of immune tolerance in NMOSD and MOGAD.
Review in Therapeutic advances in neurological disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
5 citing papers in PubMed.
- Review
- The emerging role of B cells in immune-mediated demyelinating diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- A-to-I RNA editing profiles and distinct immune responses in myelin oligodendrocyte glycoprotein antibody-positive optic neuritis.Frontiers in immunology · 2026Article
- Neuromyelitis optica spectrum disorders.Therapeutic advances in neurological disorders · 2026Article
- Astrocyte-derived extracellular vesicles as antigen-specific therapy for neuromyelitis optica spectrum disorder in the mouse model.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are autoimmune diseases characterized by immune-mediated damage to the central nervous system. Current treatments primarily focus on chronic immunosuppression. Immune tolerance induction offers a novel approach to restoring immune balance while minimizing systemic side effects. Central and peripheral immune tolerance mechanisms regulate autoreactive lymphocytes, ensuring immune homeostasis. Dysregulation of these pathways underpins NMOSD and MOGAD pathogenesis. Antigen-specific therapies targeting aquaporin-4 (AQP4) or myelin oligodendrocyte glycoprotein (MOG) autoantigens include peptide-based vaccines and nanoparticle delivery systems, promoting T cell anergy and regulatory T cell (Treg) expansion. Cell-based therapies utilizing ex vivo-expanded Tregs or regulatory B cells (Bregs) have shown promise in preclinical models but face challenges in clinical translation due to scalability and safety concerns. Gene-editing technologies such as CRISPR/Cas9 present opportunities to modulate immune pathways and restore tolerance, although delivery and off-target effects remain obstacles. Additionally, strategies addressing double-seronegative NMOSD, which lacks detectable autoantibodies, emphasize broad immune modulation rather than antigen specificity. While significant progress has been achieved, the transition to clinical application requires overcoming hurdles such as optimizing antigen delivery, ensuring long-term efficacy, and identifying reliable biomarkers. Advances in personalized medicine hold promise for achieving sustained remission, reducing dependency on immunosuppression, and improving patient outcomes in NMOSD and MOGAD. This review explores advancements in tolerance strategies, highlighting their potential in NMOSD and MOGAD.
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Registered trials
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.