ArticleThe Journal of clinical investigation2019
Anti-Neurofascin-155 IgG4 antibodies prevent paranodal complex formation in vivo.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 3 syntheses or guidelines pooled it, 102 citations in OpenAlex.
- Comparative efficacy, safety, and functional recovery of neonatal fc receptor inhibitors and conventional immunotherapies for chronic inflammatory demyelinating polyradiculoneuropathy: a systematic review and network meta-analysis.Frontiers in immunology · 2026Pooled it
- A Systematic Review and Meta-Analysis of Autoantibodies for Diagnosis and Prognosis in Patients With Chronic Inflammatory Demyelinating Polyradiculoneuropathy.Frontiers in neuroscience · 2021Pooled it
- Efficacy and safety of anti-CD20 monoclonal antibody therapy for autoimmune nodopathies: a systematic review and meta-analysis.Frontiers in neurologyPooled it
- Comparative Analytical Performance of Autoimmune Nodopathy Diagnostic Assays.Annals of laboratory medicine · 2026Article
- Characterizing Combined Central and Peripheral Demyelination-Insights From a Multimodal Comparison With Chronic Inflammatory Demyelinating Polyneuropathy and Multiple Sclerosis.Muscle & nerve · 2026Article
- Anti-GLDN antibody-associated CIDP (nodopathy): transient IVIg response and B-cell depletion remission.BMC neurology · 2026Article
- Clinical utility of human leukocyte antigen genotyping and immunoglobulin G4 autoantibody testing in autoimmune neurological diseases: A focused minireview.World journal of biological chemistry · 2026Review
- Distinct Epitopes Are Associated With Clinical Phenotypes in Autoimmune Nodopathies With Anti-Contactin1 Autoantibodies.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Clinical Spectrum, Pathology, and Mechanisms of Anti-LGI4 Antibody-Positive Autoimmune Nodopathy.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- The changing landscape of primary autoimmune neuropathies.Nature reviews. Neurology · 2025Review
- Epitope Mapping of Anti-Neurofascin 155 Antibody in a Large Cohort of Autoimmune Nodopathy Patients.Annals of clinical and translational neurology · 2025Article
- Procedure for Reliable and Long-Lasting Ex Vivo Recordings of Sciatic Nerve Activity in Mice.Bio-protocol · 2025Article
- Super-resolution of nodal and paranodal disruption in anti-pan-neurofascin-associated autoimmune nodopathy.Frontiers in immunology · 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
- Review
- Anti-neurofascin-155 antibody mediated a distinct phenotype of chronic inflammatory demyelinating polyradiculoneuropathy.Journal of neurology · 2024Article
- Peripheral Nervous System (PNS) Myelin Diseases.Cold Spring Harbor perspectives in biology · 2024Review
- Exploring the depths of IgG4: insights into autoimmunity and novel treatments.Frontiers in immunology · 2024Review
- IgG4 autoantibodies and autoantigens in the context of IgG4-autoimmune disease and IgG4-related disease.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurofascin-155 (Nfasc155) is an essential glial cell adhesion molecule expressed in paranodal septate-like junctions of peripheral and central myelinated axons. The genetic deletion of Nfasc155 results in the loss of septate-like junctions and in conduction slowing. In humans, IgG4 antibodies against Nfasc155 are implicated in the pathogenesis of chronic inflammatory demyelinating polyneuropathy (CIDP). These antibodies are associated with an aggressive onset, a refractoriness to intravenous immunoglobulin, and tremor of possible cerebellar origin. Here, we examined the pathogenic effects of patient-derived anti-Nfasc155 IgG4. These antibodies did not inhibit the ability of Nfasc155 to complex with its axonal partners contactin-1/CASPR1 or induce target internalization. Passive transfer experiments revealed that IgG4 antibodies target Nfasc155 on Schwann cell surface, and diminished Nfasc155 protein levels and prevented paranodal complex formation in neonatal animals. In adult animals, chronic intrathecal infusions of antibodies also induced the loss of Nfasc155 and of paranodal specialization and resulted in conduction alterations in motor nerves. These results indicate that anti-Nfasc155 IgG4 perturb conduction in absence of demyelination, validating the existence of paranodopathy. These results also shed light on the mechanisms regulating protein insertion at paranodes.
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Registered trials
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.