ArticleThe Journal of biological chemistry2014
Specific contactin N-glycans are implicated in neurofascin binding and autoimmune targeting in peripheral neuropathies.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Efficacy and safety of anti-CD20 monoclonal antibody therapy for autoimmune nodopathies: a systematic review and meta-analysis.Frontiers in neurologyPooled it
- Glycosylation profile ofiScience · 2026Article
- Neurofascin Antibodies in a Large Cohort of Inflammatory Neuropathies from India.Annals of Indian Academy of Neurology · 2026Article
- Specific HLA-DRB1 Alleles Associate With Anti-Caspr1 and Anti-CNTN1 Autoantibodies in Autoimmune Nodopathies.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Characteristics of pediatric-onset anti-contactin1 antibody-associated autoimmune nodopathies with concomitant membranous nephropathy.BMC pediatrics · 2026Review
- Distinct Epitopes Are Associated With Clinical Phenotypes in Autoimmune Nodopathies With Anti-Contactin1 Autoantibodies.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Advances in the treatment of autoimmune nodopathy: based on treatment strategies of CIDP.Frontiers in immunology · 2026Review
- Epitope Mapping of Anti-Neurofascin 155 Antibody in a Large Cohort of Autoimmune Nodopathy Patients.Annals of clinical and translational neurology · 2025Article
- The Discovery of Autoimmune Nodopathies and the Impact of IgG4 Antibodies in Autoimmune Neurology.Neurology(R) neuroimmunology & neuroinflammation · 2025Review
- Antibody-Mediated Nodo- and Paranodopathies.Journal of clinical medicine · 2024Review
- IgG4 autoantibodies and autoantigens in the context of IgG4-autoimmune disease and IgG4-related disease.Frontiers in immunology · 2024Review
- Recurrent CNTN1 antibody-positive nodopathy: a case report and literature review.Frontiers in immunology · 2024Review
- The unique properties of IgG4 and its roles in health and disease.Nature reviews. Immunology · 2023Review
- Anti-pan-neurofascin antibodies induce subclass-related complement activation and nodo-paranodal damage.Brain : a journal of neurology · 2023Article
- Growing Spectrum of Autoimmune Nodopathies.Current neurology and neuroscience reports · 2023Review
- Glycine receptor autoantibody binding to the extracellular domain is independent from receptor glycosylation.Frontiers in molecular neuroscience · 2023Article
- Different binding and pathogenic effect of neurofascin and contactin-1 autoantibodies in autoimmune nodopathies.Frontiers in immunology · 2023Article
- Pathology of Initial Axon Segments in Chronic Inflammatory Demyelinating Polyradiculoneuropathy and Related Disorders.International journal of molecular sciences · 2022Review
- Structural insights into the contactin 1 - neurofascin 155 adhesion complex.Nature communications · 2022Article
- IgG4 Valency Modulates the Pathogenicity of Anti-Neurofascin-155 IgG4 in Autoimmune Nodopathy.Neurology(R) neuroimmunology & neuroinflammation · 2022Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell adhesion molecules (CAMs) play a crucial role in the formation of the nodes of Ranvier and in the rapid propagation of the nerve impulses along myelinated axons. These CAMs are the targets of autoimmunity in inflammatory neuropathies. We recently showed that a subgroup of patients with aggressive chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) shows autoantibodies to contactin (1). The complex of contactin·Caspr·neurofascin-155 (NF155) enables the formation of paranodal junctions, suggesting that antibody attack against paranodes may participate in the severity of CIDP. In the present study, we mapped the molecular determinants of contactin targeted by the autoantibodies. In three patients, immunoreactivity was directed against the Ig domains of contactin and was dependent on N-glycans. The serum of one patient was selectively directed against contactin bearing mannose-rich N-glycans. Strikingly, the oligomannose type sugars of contactin are required for association with its glial partner NF155 (2). To investigate precisely the role of contactin N-glycans, we have mutated each of the nine consensus N-glycosylation sites independently. We found that the mutation of three sites (N467Q/N473Q/N494Q) in Ig domain 5 of contactin prevented soluble NF155-Fc binding. In contrast, these mutations did not abolish cis-association with Caspr. Next, we showed that the cluster of N-glycosylation sites (Asn-467, Asn-473, and Asn-494) was required for immunoreactivity in one patient. Using cell aggregation assays, we showed that the IgGs from the four CIDP patients prevented adhesive interaction between contactin·Caspr and NF155. Importantly, we showed that the anti-contactin autoantibodies induced alteration of paranodal junctions in myelinated neuronal culture. These results strongly suggest that antibodies to CAMs may be pathogenic and induce demyelination via functional blocking activity.
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