ArticleFrontiers in immunology2024
Differentiated pattern of complement system activation between MOG-IgG-associated disease and AQP4-IgG-positive neuromyelitis optica spectrum disorder.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS.Annals of clinical and translational neurology · 2026Article
- Subclinical neurovascular and immune correlates of post-COVID-19 syndrome detected by retinal imaging.Brain, behavior, & immunity - health · 2026Article
- The Effects of Fermented Chinese Herbal Medicine on Growth Performance, Immunity, Intestinal Microbiota, and Intestinal Metabolite Profile of Broiler Chicks.Probiotics and antimicrobial proteins · 2026Article
- Characteristic patterns of complement deposition in NMOSD, MOGAD, and MS.Acta neuropathologica · 2026Article
- Emerging role of complement system in the induction of neuroinflammation in adenylosuccinate lyase deficiency disorder.Brain, behavior, & immunity - health · 2025Review
- A case of MOGAD with rectal adenocarcinoma: Comorbidity or paraneoplastic neurological syndrome?Brain, behavior, & immunity - health · 2025Article
- Immunoglobulin G and Complement as Major Players in the Neurodegeneration of Multiple Sclerosis.Biomolecules · 2024Review
- Different Complement Activation Patterns Following C5 Cleavage in MOGAD and AQP4-IgG+NMOSD.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
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Authors and funding
21 authors at 16 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Myelin oligodendrocyte glycoprotein antibody (MOG) immunoglobulin G (IgG)-associated disease (MOGAD) has clinical and pathophysiological features that are similar to but distinct from those of aquaporin-4 antibody (AQP4-IgG)-positive neuromyelitis optica spectrum disorders (AQP4-NMOSD). MOG-IgG and AQP4-IgG, mostly of the IgG1 subtype, can both activate the complement system. Therefore, we investigated whether the levels of serum complement components, regulators, and activation products differ between MOGAD and AQP4-NMOSD, and if complement analytes can be utilized to differentiate between these diseases. Methods: The sera of patients with MOGAD (from during an attack and remission; Results: In attack samples, the levels of C1-INH, FH, and iC3b were higher in the MOGAD group than in the NMOSD group (all, Conclusions: This study indicates a higher prominence of complement pathway activation and subsequent C3 degradation in MOGAD compared to AQP4-NMOSD. On the other hand, the production of terminal complement complexes (TCC) was found to be more substantial in AQP4-NMOSD than in MOGAD. These findings suggest a strong regulation of the complement system, implying its potential involvement in the pathogenesis of MOGAD through mechanisms that extend beyond TCC formation.
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