ArticleFrontiers in immunology2023
Patients' IgLON5 autoantibodies interfere with IgLON5-protein interactions.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.
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.
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Who cites it
22 citing papers in PubMed, 24 citations in OpenAlex.
- Structural basis of IgLON5 autoantibody recognition in autoimmune encephalitis.Nature communications · 2026Article
- The cascade to pathogenicity in autoantibody-mediated CNS diseases.Brain : a journal of neurology · 2026Review
- Muscle Regeneration Failure May Lead to Clinical Features of Myopathy in Anti-IgLON5 Disease.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Synaptophysin autoantibodies mediate synaptic dysfunction in cerebellar ataxia.Cell reports. Medicine · 2026Article
- Anti-IgLON5 encephalitis is associated with anti-retinal immunological reactivity without retinal alteration.Journal of translational autoimmunity · 2026Article
- IgLON5 autoimmune antibodies activate Tau via neuronal hyperactivity.Science advances · 2026Article
- Brainstem pathology in anti-IgLON5 disease: new insights into early events and tau progression.Brain : a journal of neurology · 2026Article
- A patient with anti-IgLON5 disease associated with cerebral hemorrhage, multiple ischemic strokes, and kidney failure: case report.Journal of neurology · 2026Article
- Anti-IgLON5 disease presenting with myokymia and favourable response to FcRN-antagonist combined with oral glucocorticoids: case report.Frontiers in immunology · 2026Article
- Cytoskeletal disruption-induced calcium dysregulation drives cell death in anti-IgLON5 disease.Redox biology · 2025Article
- Neurodegeneration and the immune system: lessons from autoimmune encephalitis.Journal of neurology · 2025Review
- Anti-IgLON5 Disease 10 Years Later: What We Know and What We Do Not Know.Neurology(R) neuroimmunology & neuroinflammation · 2025Review
- Neuropathological spectrum of anti-IgLON5 disease and stages of brainstem tau pathology: updated neuropathological research criteria of the disease-related tauopathy.Acta neuropathologica · 2024Article
- The presence and clinical significance of autoantibodies in amyotrophic lateral sclerosis: a narrative review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Review
- Antibodies Against ZSCAN1 in Pediatric and Adult Patients With Non-Paraneoplastic ROHHAD Syndrome.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- IgLON5-IgG: Innocent Bystander or Perpetrator?International journal of molecular sciences · 2024Review
- HLA dependency and possible clinical relevance of intrathecally synthesized anti-IgLON5 IgG4 in anti-IgLON5 disease.Frontiers in immunology · 2024Article
- IgLON5 autoimmunity in a patient with Creutzfeldt-Jakob disease: case report and review of literature.Frontiers in neurology · 2024Article
- IgLON5 deficiency produces behavioral alterations in a knockout mouse model.Frontiers in immunology · 2024Article
- Analysis of inflammatory markers and tau deposits in an autopsy series of nine patients with anti-IgLON5 disease.Acta neuropathologica · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Background: Anti-IgLON5 disease is a rare neurological disorder characterized by autoantibodies against IgLON5, and pathological evidence of neurodegeneration. IgLON5 is a cell adhesion molecule but its physiological function is unknown. Our aim was to investigate the IgLON5 interactome and to determine if IgLON5 antibodies (IgLON5-abs) affect these protein interactions. Methods: IgLON5 interactome was investigated by mass spectrometry sequencing of proteins immunoprecipitated by IgLON5 autoantibodies using cultures of rat cerebellar granular neurons (CGNs). Shedding of IgLON5 was explored using HEK cells transfected with human IgLON5 plasmid and in CGNs. Interactions of IgLON5 with identified binding partners and IgLON5-abs effects were confirmed by immunofluorescence in transfected HEK cells and rat hippocampal neurons. Results: Patients' IgLON5 antibodies co-precipitated all members of the IgLON family and three 3 additional surface proteins. IgLON5 predominantly establishes homomeric and heteromeric Conclusions: We show a potentially novel pathogenic mechanism of IgLON5-abs that consists in blocking IgLON5 interactions with its binding partners. These findings extend our knowledge about the physiological role of IgLON5 and pave the way to future understanding of the pathological mechanisms of anti-IgLON5 disease.
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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.