ArticleJournal of neurology2024
IgG subclass shifts occurring at acute exacerbations in autoimmune nodopathies.
Article in Journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Serum PLA2R-IgG4/PLA2R-IgG ratio dynamics reveal pathogenic autoantibody subclass switch during progression of PLA2R-associated membranous nephropathy.Annals of medicine · 2026Article
- Beyond Chronic Inflammatory Demyelinating Polyradiculoneuropathy: Anti-Contactin-1 Autoimmune Nodopathy Unmasked by Proteinuria.Journal of clinical medicine · 2026Article
- Characteristics of pediatric-onset anti-contactin1 antibody-associated autoimmune nodopathies with concomitant membranous nephropathy.BMC pediatrics · 2026Review
- Clinical Spectrum, Pathology, and Mechanisms of Anti-LGI4 Antibody-Positive Autoimmune Nodopathy.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Case report: target antigen and subclass switch in a patient with autoimmune nodopathy.Frontiers in immunology · 2024Article
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Authors and funding
9 authors.
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Abstract
backgroundAutoimmune nodopathy associated with anti-contactin1 (CNTN1) IgG4 antibodies frequently manifests as acute axonal degeneration in addition to detachment of the paranodal myelin loops. The acute destruction of myelinated nerve fibers does not match the function of IgG4, which cannot activate the complement pathway. IgG subclass switching from IgG1 or IgG3 to IgG4 has been observed in some patients with autoimmune diseases associated with IgG4 throughout their disease course.
methodsSerial changes in IgG subclasses, clinico-neurophysiological features, and nerve and renal pathology were reviewed in three patients with anti-CNTN1-associated autoimmune nodopathy and one patient with anti-contactin-associated protein1 (Caspr1) autoimmune nodopathy.
resultsAll four patients had predominantly IgG4 autoantibodies, whereas they showed evidence of acute axonal degeneration. The IgG1 subclass was present in all patients at their progressing stage but then disappeared at follow-up. Nerve pathology in the patients with anti-CNTN1 and anti-Caspr1 autoimmune nodopathies showed both structural changes in the paranodes and evidence of acute axonal degeneration. Renal biopsy specimens from two patients with membranous glomerulonephritis and anti-CNTN1 autoimmune nodopathy showed deposition of IgG1 and complement on the glomerular basement membrane, as well as IgG4. DISCUSSION: In patients with autoimmune nodopathies associated with anti-CNTN1 and anti-Caspr1 IgG4 antibodies, IgG1 subclass autoantibodies were present at their acute exacerbations and might have contributed to the axonal degeneration and glomerular injury. IgG1 disappeared with the cessation of disease progression, which indicates that the IgG1 subclass is a possible biomarker of disease activity.
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