ArticleNeurology(R) neuroimmunology & neuroinflammation2026
Patient-Derived Monoclonal Myelin Oligodendrocyte Glycoprotein Autoantibodies Mediate Cytotoxicity.
Article in Neurology(R) neuroimmunology & neuroinflammation, 2026. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Human Autoantibodies Against MOG Isoforms: α3 Antibodies Suggest Relapsing Disease Course in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- The cascade to pathogenicity in autoantibody-mediated CNS diseases.Brain : a journal of neurology · 2026Review
- Use of Fluid Biomarkers in NMOSD and MOGAD: Clinical and Research Applications.Neurology(R) neuroimmunology & neuroinflammation · 2026Review
- Beyond Positivity: Understanding and Interpreting MOG-IgG Testing in MOGAD.Journal of clinical neurology (Seoul, Korea) · 2026Review
- Generation of Monoclonal Autoantibodies From Myelin Oligodendrocyte Glycoprotein-Specific Human B Cells Using an Optofluidic-Based Platform.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
BACKGROUND AND
objectivesSerum myelin oligodendrocyte glycoprotein (MOG) antibodies are a hallmark of the newly defined neuroinflammatory disease entity MOG antibody-associated disease (MOGAD). Yet, the lack of patient-derived recombinant human MOG (hMOG)-reactive autoantibodies limits investigations into the molecular mechanisms by which these autoantibodies mediate CNS pathology, thereby hindering rational therapeutic approaches. To understand the origins and disease-relevant mechanisms of autoantibodies in MOGAD, we generated and characterized monoclonal anti-hMOG antibodies (MOG-mAbs) from circulating B cells of patients with MOGAD.
methodsWe isolated MOG-specific B-cell receptor (BCR) sequences from unique circulating B-cell clones of 6 patients with MOGAD using an antigen selection approach. BCR sequences were expressed as immunoglobulin (Ig)G1 antibodies, and their molecular features, epitope specificity, and binding to MOG isoforms were investigated. The MOG-mAbs' ability to mediate antibody-dependent cellular phagocytosis (ADCP), natural killer (NK) cell-mediated antibody-dependent cellular cytotoxicity (ADCC), and complement-dependent cytotoxicity (CDC) toward MOG-expressing cells was assessed by live cell-based assays.
resultsOf the 15 MOG-mAbs generated, 4 revealed evidence of affinity maturation, whereas the remaining 11 were germline encoded. Binding capacities to hMOG varied considerably, with the most frequent putative epitope mapping to a region that includes residue P42. The efficacy of these antibodies in mediating ADCP, ADCC, and CDC of MOG-expressing cells was heterogeneous and associated with their binding characteristics to MOG and its isoforms. DISCUSSION: Taken together, the molecular characteristics and binding patterns of these patient-derived MOG-mAbs reveal a diverse repertoire of MOG-binding autoantibodies with pathogenic capacity in vitro. Consequently, these well-characterized patient autoantibodies offer a foundation for developing in vivo models of MOGAD, serve as tools to standardize diagnostic assays, and guide development of therapeutic strategies targeting either B cells or autoantibodies and their effector functions.
Indexed as
Identifiers
What OpenQuestion holds
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.