ArticleFrontiers in cellular neuroscience2015
Inhibitory axons are targeted in hippocampal cell culture by anti-Caspr2 autoantibodies associated with limbic encephalitis.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 67 citations in OpenAlex.
- Contrasting Outcomes in Two Cases of Anti-contactin-associated Protein-like 2 Autoimmune Encephalitis.Internal medicine (Tokyo, Japan) · 2026Article
- CNTNAP2: isoform- and context-specific functions in neurological disorders and cancer.Frontiers in cellular neuroscience · 2026Review
- Neuromyotonia and CASPR2 Antibodies: Electrophysiological Clues to Disease Pathophysiology.Biomolecules · 2025Review
- Human cerebrospinal fluid monoclonal CASPR2 autoantibodies induce changes in electrophysiology, functional MRI, and behavior in rodent models.Brain, behavior, and immunity · 2024Article
- Molecular mechanism of contactin 2 homophilic interaction.Structure (London, England : 1993) · 2024Article
- Review
- Differential impacts ofFrontiers in neuroscience · 2023Article
- Autoimmune Encephalitis in COVID-19 Infection: Our Experience and Systematic Review of the Literature.Biomedicines · 2022Review
- Distinctive clinical presentation and pathogenic specificities of anti-AK5 encephalitis.Brain : a journal of neurology · 2021Article
- Genome-wide variant-based study of genetic effects with the largest neuroanatomic coverage.BMC bioinformatics · 2021Article
- Clinical Character of CASPR2 Autoimmune Encephalitis: A Multiple Center Retrospective Study.Frontiers in immunology · 2021Article
- Assembly and Function of the Juxtaparanodal Kv1 Complex in Health and Disease.Life (Basel, Switzerland) · 2020Review
- Cognitive impact of neuronal antibodies: encephalitis and beyond.Translational psychiatry · 2020Review
- Decreased amplitude and reliability of odor-evoked responses in two mouse models of autism.Journal of neurophysiology · 2020Article
- Diagnostic Value of Structural and Functional Neuroimaging in Autoimmune Epilepsy.Contrast media & molecular imaging · 2020Review
- Autoimmune seizures and epilepsy.The Journal of clinical investigation · 2019Review
- Selective Axonal Expression of the Kv1 Channel Complex in Pre-myelinated GABAergic Hippocampal Neurons.Frontiers in cellular neuroscience · 2019Article
- A New Classification System for IgG4 Autoantibodies.Frontiers in immunology · 2018Review
- Autoantibodies Against the Node of Ranvier in Seropositive Chronic Inflammatory Demyelinating Polyneuropathy: Diagnostic, Pathogenic, and Therapeutic Relevance.Frontiers in immunology · 2018Review
- Mechanisms of Caspr2 antibodies in autoimmune encephalitis and neuromyotonia.Annals of neurology · 2018Article
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Contactin-associated protein-like 2 (Caspr2), also known as CNTNAP2, is a cell adhesion molecule that clusters voltage-gated potassium channels (Kv1.1/1.2) at the juxtaparanodes of myelinated axons and may regulate axonal excitability. As a component of the Kv1 complex, Caspr2 has been identified as a target in neuromyotonia and Morvan syndrome, but also in some cases of autoimmune limbic encephalitis (LE). How anti-Caspr2 autoimmunity is linked with the central neurological symptoms is still elusive. In the present study, using anti-Caspr2 antibodies from seven patients affected by pure LE, we determined that IgGs in the cerebrospinal fluid of four out seven patients were selectively directed against the N-terminal Discoïdin and LamininG1 modules of Caspr2. Using live immunolabeling of cultured hippocampal neurons, we determined that serum IgGs in all patients strongly targeted inhibitory interneurons. Caspr2 was highly detected on GAD65-positive axons that are surrounding the cell bodies and at the VGAT-positive inhibitory presynaptic contacts. Functional assays indicated that LE autoantibodies may induce alteration of Gephyrin clusters at inhibitory synaptic contacts. Next, we generated a Caspr2-Fc chimera to reveal Caspr2 receptors on hippocampal neurons localized at the somato-dendritic compartment and post-synapse. Caspr2-Fc binding was strongly increased on TAG-1-transfected neurons and conversely, Caspr2-Fc did not bind hippocampal neurons from TAG-1-deficient mice. Our data indicate that Caspr2 may participate as a cell recognition molecule in the dynamics of inhibitory networks. This study provides new insight into the potential pathogenic effect of anti-Caspr2 autoantibodies in central hyperexcitability that may be related with perturbation of inhibitory interneuron activity.
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