ArticleBrain, behavior, and immunity2024
Human cerebrospinal fluid monoclonal CASPR2 autoantibodies induce changes in electrophysiology, functional MRI, and behavior in rodent models.
Abstract read
In one paragraph
Article in Brain, behavior, and immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
11 citing papers in PubMed.
- Associations of viral infections and antiviral vaccinations with anti-NMDAR and other forms of autoimmune encephalitis.Brain, behavior, & immunity - health · 2026Review
- The cascade to pathogenicity in autoantibody-mediated CNS diseases.Brain : a journal of neurology · 2026Review
- Recent advances in autoantibody-mediated pain.Current opinion in supportive and palliative care · 2026Review
- High-Affinity Human Germline and Mutated Autoantibodies Commonly Cross-React to Self-Antigens in 5 Subgroups of Autoimmune Encephalitis.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- AMPAR immunization induces progressive autoimmune encephalitis with autoreactive B cells in the brain.bioRxiv : the preprint server for biology · 2026Article
- CASPR2 Autoimmune Antibodies Induce Neuronal Hyperactivity in Human Brain Organoids.Journal of neurochemistry · 2026Article
- Immunopathological mechanisms in autoimmune encephalitis: from pathogenesis to targeted therapies.Frontiers in immunology · 2026Review
- Heterogeneity of anti-Caspr2 antibodies: specificity and pathogenicity.Translational psychiatry · 2025Article
- Activated αβ T and reduced mucosa-associated invariant T cells in LGI1- and CASPR2-encephalitis.Brain : a journal of neurology · 2025Article
- Neurodegeneration and the immune system: lessons from autoimmune encephalitis.Journal of neurology · 2025Review
- Antibodies in neurological diseases: Established, emerging, explorative.Immunological reviews · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Scott van HoofGerman Center for Neurodegenerative Diseases (DZNE) Berlin, 10117 Berlin, Germany; Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany; Helmholtz Innovation Lab BaoBab (Brain Antibody-omics and B-cell Lab), Berlin, Germany.
Jakob KreyeGerman Center for Neurodegenerative Diseases (DZNE) Berlin, 10117 Berlin, Germany; Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany; Helmholtz Innovation Lab BaoBab (Brain Antibody-omics and B-cell Lab), Berlin, Germany; Department of Pediatric Neurology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany; Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany.
César Cordero-GómezGerman Center for Neurodegenerative Diseases (DZNE) Berlin, 10117 Berlin, Germany; Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany.
Julius HoffmannGerman Center for Neurodegenerative Diseases (DZNE) Berlin, 10117 Berlin, Germany; Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany.
S Momsen ReinckeGerman Center for Neurodegenerative Diseases (DZNE) Berlin, 10117 Berlin, Germany; Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany; Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany.
Elisa Sánchez-SendinGerman Center for Neurodegenerative Diseases (DZNE) Berlin, 10117 Berlin, Germany; Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany; Helmholtz Innovation Lab BaoBab (Brain Antibody-omics and B-cell Lab), Berlin, Germany.
Sophie L DuongGerman Center for Neurodegenerative Diseases (DZNE) Berlin, 10117 Berlin, Germany; Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany.
Manoj UpadhyaInstitute of Health and Neurodevelopment, College of Health and Life Sciences, Aston University, Birmingham, UK.
Divya DhangarInstitute of Health and Neurodevelopment, College of Health and Life Sciences, Aston University, Birmingham, UK.
Paulina MichórInstitute of Health and Neurodevelopment, College of Health and Life Sciences, Aston University, Birmingham, UK.
Gavin L WoodhallInstitute of Health and Neurodevelopment, College of Health and Life Sciences, Aston University, Birmingham, UK.
Maraike KüpperOscar Langendorff Institute of Physiology, University of Rostock, Germany, Center of Transdisciplinary Neurosciences Rostock (CTNR), Germany.
Andreas OderScreening Unit, Leibniz Forschungsinstitut für Molekulare Pharmakologie, 13125 Berlin, Germany.
Joseph KuchlingDepartment of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany; Neurocure Cluster of Excellence, NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany.
Stefan Paul KochDepartment of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany; Center for Stroke Research Charité Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; NeuroCure Cluster of Excellence and Charité Core Facility 7T Experimental MRIs, Charité - Universitätsmedizin Berlin, Germany; Charité 3R, Replace, Reduce, Refine, Charité - Universitätsmedizin Berlin, Germany.
Susanne MuellerDepartment of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany; Center for Stroke Research Charité Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; NeuroCure Cluster of Excellence and Charité Core Facility 7T Experimental MRIs, Charité - Universitätsmedizin Berlin, Germany; Charité 3R, Replace, Reduce, Refine, Charité - Universitätsmedizin Berlin, Germany.
Philipp Boehm-SturmDepartment of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany; Center for Stroke Research Charité Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; NeuroCure Cluster of Excellence and Charité Core Facility 7T Experimental MRIs, Charité - Universitätsmedizin Berlin, Germany; Charité 3R, Replace, Reduce, Refine, Charité - Universitätsmedizin Berlin, Germany.
Jens Peter von KriesScreening Unit, Leibniz Forschungsinstitut für Molekulare Pharmakologie, 13125 Berlin, Germany.
Carsten FinkeDepartment of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany; Neurocure Cluster of Excellence, NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany.
Timo KirschsteinOscar Langendorff Institute of Physiology, University of Rostock, Germany, Center of Transdisciplinary Neurosciences Rostock (CTNR), Germany.
Sukhvir K WrightInstitute of Health and Neurodevelopment, College of Health and Life Sciences, Aston University, Birmingham, UK; Department of Paediatric Neurology, The Birmingham Women's and Children's Hospital National Health Service Foundation Trust, Birmingham, UK.
Harald PrüssGerman Center for Neurodegenerative Diseases (DZNE) Berlin, 10117 Berlin, Germany; Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, 10117 Berlin, Germany; Helmholtz Innovation Lab BaoBab (Brain Antibody-omics and B-cell Lab), Berlin, Germany. Electronic address: harald.pruess@charite.de.
Funding
Wellcome Trust 216613
Abstract
Anti-contactin associated protein receptor 2 (CASPR2) encephalitis is a severe autoimmune encephalitis with a variable clinical phenotype including behavioral abnormalities, cognitive decline, epileptic seizures, peripheral nerve hyperexcitability and neuropathic pain. The detailed mechanisms of how CASPR2 autoantibodies lead to synaptic dysfunction and clinical symptoms are largely unknown. Aiming for analyses from the molecular to the clinical level, we isolated antibody-secreting cells from the cerebrospinal fluid of two patients with CASPR2 encephalitis. From these we cloned four anti-CASPR2 human monoclonal autoantibodies (mAbs) with strong binding to brain and peripheral nerves. All were highly hypermutated and mainly of the IgG4 subclass. Mutagenesis studies determined selective binding to the discoidin domain of CASPR2. Surface plasmon resonance revealed affinities with dissociation constants K
Indexed as
Antibodies, MonoclonalAutoantibodiesEncephalitisMagnetic Resonance ImagingMembrane ProteinsNerve Tissue ProteinsAnimalsBehavior, AnimalBrainDisease Models, AnimalFemaleHippocampusHumansMaleMiceRatsAntibodies, MonoclonalAutoantibodiesCNTNAP2 protein, humanMembrane ProteinsNerve Tissue ProteinsAutoantibodiesAutoimmune encephalitisCASPR2Human monoclonal antibodyMouse MRI
Identifiers
What OpenQuestion holds
Textmetadata
LicenceCC BY
Read underepoch 390
Registered trials
None linked
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.