ArticleNeurology(R) neuroimmunology & neuroinflammation2026
Distinct Epitopes Are Associated With Clinical Phenotypes in Autoimmune Nodopathies With Anti-Contactin1 Autoantibodies.
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 2 papers.
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Who cites it
2 citing papers in PubMed.
- Conformational stability and domain-specific structural features of tumor autoantigens regulate autoantibody epitope propensity.Protein science : a publication of the Protein Society · 2026Article
- Polyclonal glycine receptor aAbs: a challenge for personalized epitope characterization.Frontiers in molecular neuroscience · 2026Article
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Authors and funding
16 authors.
Funding
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Abstract
BACKGROUND AND
objectivesAutoimmune nodopathy with anti-contactin1 (CNTN1) autoantibodies is a rare sensory-motor neuropathy characterized by subacute-onset sensory ataxia and variable disease courses. Comorbidities such as glomerulonephritis and diabetes mellitus are observed in some patients. The diversity in clinical presentation may reflect differences in the targeted CNTN1 epitopes.
methodsTo investigate the relationship between clinical features and the underlying epitopes, we analyzed serum samples from 16 anti-CNTN1-positive patients. Binding epitopes were assessed using cell-based assays with recombinant CNTN1 variants and peptide microarrays.
resultsEpitope mapping in 16 patients revealed that 13 harbored antibodies targeting CNTN1 immunoglobulin (Ig) domains while 3 recognized fibronectin (Fn) domains. Glomerulonephritis was exclusively observed in patients with autoantibodies binding to the Ig domain, whereas diabetes mellitus and a chronic course of disease were more prevalent in patients with binding to the fibronectin domain. DISCUSSION: Our findings highlight the heterogeneity of anti-contactin1 nodopathies, suggesting that distinct epitope-binding patterns may underlie different clinical manifestations and may be associated with different pathogenic mechanisms and comorbidities.
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