ArticleMolecular pharmacology2013
Therapeutic cleavage of anti-aquaporin-4 autoantibody in neuromyelitis optica by an IgG-selective proteinase.
Article in Molecular pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 64 citations in OpenAlex.
- Trial
- Polypharmacology of S-1117, an Fc-fused IgG-selective degrading enzyme, for chronic treatment of autoantibody-mediated diseases.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Novel assays to assess the prevalence and neutralizing potential of anti-IdeS antibodies in healthy humans.Frontiers in immunology · 2026Article
- Therapeutic IgG- and IgM-specific proteases disarm the acetylcholine receptor autoantibodies that drive myasthenia gravis pathology.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Diagnosing and Managing Uveitis Associated with Immune Checkpoint Inhibitors: A Review.Diagnostics (Basel, Switzerland) · 2024Review
- 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
- Neuromyelitis Optica Spectrum Disorder Treatment-Current and Future Prospects.International journal of molecular sciences · 2021Review
- New Therapeutic Landscape in Neuromyelitis Optica.Current treatment options in neurology · 2021Review
- Monoclonal Antibody-Based Treatments for Neuromyelitis Optica Spectrum Disorders: From Bench to Bedside.Neuroscience bulletin · 2020Review
- Article
- Emerging therapeutic targets for neuromyelitis optica spectrum disorder.Expert opinion on therapeutic targets · 2020Review
- Affinity-matured 'aquaporumab' anti-aquaporin-4 antibody for therapy of seropositive neuromyelitis optica spectrum disorders.Neuropharmacology · 2020Article
- 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
- Bystander mechanism for complement-initiated early oligodendrocyte injury in neuromyelitis optica.Acta neuropathologica · 2017Article
- Impact of Desensitization on Antiviral Immunity in HLA-Sensitized Kidney Transplant Recipients.Journal of immunology research · 2017Article
- The Bacterial Enzyme IdeS Cleaves the IgG-Type of B Cell Receptor (BCR), Abolishes BCR-Mediated Cell Signaling, and Inhibits Memory B Cell Activation.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the central nervous system caused by binding of pathogenic IgG autoantibodies (NMO-IgG) to astrocyte water channel aquaporin-4 (AQP4). Astrocyte damage and downstream inflammation require NMO-IgG effector function to initiate complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC). Here, we evaluated the potential therapeutic utility of the bacterial enzyme IdeS (IgG-degrading enzyme of Streptococcus pyogenes), which selectively cleaves IgG antibodies to yield Fc and F(ab')(2) fragments. In AQP4-expressing cell cultures, IdeS treatment of monoclonal NMO-IgGs and NMO patient sera abolished CDC and ADCC, even when IdeS was added after NMO-IgG was bound to AQP4. Binding of NMO-IgG to AQP4 was similar to that of the NMO-F(ab')(2) generated by IdeS cleavage. NMO-F(ab')(2) competitively displaced pathogenic NMO-IgG, preventing cytotoxicity, and the Fc fragments generated by IdeS cleavage reduced CDC and ADCC. IdeS efficiently cleaved NMO-IgG in mice in vivo, and greatly reduced NMO lesions in mice administered NMO-IgG and human complement. IgG-selective cleavage by IdeS thus neutralizes NMO-IgG pathogenicity, and yields therapeutic F(ab')(2) and Fc fragments. IdeS treatment, by therapeutic apheresis or direct administration, may be beneficial in NMO.
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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.