ArticleAnnals of neurology2013
Enzymatic deglycosylation converts pathogenic neuromyelitis optica anti-aquaporin-4 immunoglobulin G into therapeutic antibody.
Article in Annals of neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 91 citations in OpenAlex.
- Antibody glycosylation in neuroimmune diseases.Journal of translational medicine · 2025Review
- Inflammatory transcriptomic signatures in a human cellular NMOSD model reveal upregulation of NF-κB and IL6 pathways.Scientific reports · 2025Article
- Insights into neuromyelitis optica spectrum disorder and pregnancy from a single-center study in Thailand.Scientific reports · 2025Article
- Diagnosing and Managing Uveitis Associated with Immune Checkpoint Inhibitors: A Review.Diagnostics (Basel, Switzerland) · 2024Review
- Large molecules from the cerebrospinal fluid enter the optic nerve but not the retina of mice.Fluids and barriers of the CNS · 2024Article
- Reduced serum IgG galactosylation is associated with increased inflammation during relapses of neuromyelitis optica spectrum disorders.Frontiers in immunology · 2024Article
- IgG N-glycan Signatures as Potential Diagnostic and Prognostic Biomarkers.Diagnostics (Basel, Switzerland) · 2023Review
- Ocular adverse events associated with immune checkpoint inhibitors, a scoping review.Journal of ophthalmic inflammation and infection · 2023Article
- ACT001 Relieves NMOSD Symptoms by Reducing Astrocyte Damage with an Autoimmune Antibody.Molecules (Basel, Switzerland) · 2023Article
- Aquaporins in Nervous System.Advances in experimental medicine and biology · 2023Article
- Autoantibodies in neurological disease.Nature reviews. Immunology · 2021Review
- Solution structure of deglycosylated human IgG1 shows the role of CBiophysical journal · 2021Article
- B Cells and Antibodies as Targets of Therapeutic Intervention in Neuromyelitis Optica Spectrum Disorders.Pharmaceuticals (Basel, Switzerland) · 2021Review
- New Therapeutic Landscape in Neuromyelitis Optica.Current treatment options in neurology · 2021Review
- Towards middle-up analysis of polyclonal antibodies: subclass-specific N-glycosylation profiling of murine immunoglobulin G (IgG) by means of HPLC-MS.Scientific reports · 2020Article
- The history of IgG glycosylation and where we are now.Glycobiology · 2020Review
- Emerging therapeutic targets for neuromyelitis optica spectrum disorder.Expert opinion on therapeutic targets · 2020Review
- Experimental animal models of aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders: progress and shortcomings.Brain pathology (Zurich, Switzerland) · 2020Review
- Membrane assembly of aquaporin-4 autoantibodies regulates classical complement activation in neuromyelitis optica.The Journal of clinical investigation · 2019Article
- Elevated Plasma Chemokines for Eosinophils in Neuromyelitis Optica Spectrum Disorders during Remission.Frontiers in neurology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveNeuromyelitis optica (NMO) is caused by binding of pathogenic autoantibodies (NMO-immunoglobulin G [IgG]) to aquaporin-4 (AQP4) on astrocytes, which initiates complement-dependent cytotoxicity (CDC) and inflammation. We recently introduced mutated antibody (aquaporumab) and small-molecule blocker strategies for therapy of NMO, based on prevention of NMO-IgG binding to AQP4. Here, we investigated an alternative strategy involving neutralization of NMO-IgG effector function by selective IgG heavy-chain deglycosylation with bacteria-derived endoglycosidase S (EndoS).
methodsCytotoxicity and NMO pathology were measured in cell and spinal cord slice cultures, and in mice exposed to control or EndoS-treated NMO-IgG.
resultsEndoS treatment of NMO patient serum reduced by >95% CDC and antibody-dependent cell-mediated cytotoxicity, without impairment of NMO-IgG binding to AQP4. Cytotoxicity was also prevented by addition of EndoS after NMO-IgG binding to AQP4. The EndoS-treated, nonpathogenic NMO-IgG competitively displaced pathogenic NMO-IgG bound to AQP4, and prevented NMO pathology in spinal cord slice culture and mouse models of NMO.
interpretationEndoS deglycosylation converts pathogenic NMO-IgG autoantibodies into therapeutic blocking antibodies. EndoS treatment of blood may be beneficial in NMO, and may be accomplished, for example, by therapeutic apheresis using surface-immobilized EndoS.
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