ArticleAnnals of clinical and translational neurology2017
NMDAR encephalitis: passive transfer from man to mouse by a recombinant antibody.
Article in Annals of clinical and translational neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04372615 (A Phase-2b, Double-Blind, Randomized Controlled Trial to Evaluate the Activity and Safety of Inebilizumab in Anti-Nmda Receptor Encephalitis and Assess Markers of Disease), which is not on this map. Cited by 70 papers.
What it found
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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.
A Phase-2b, Double-Blind, Randomized Controlled Trial to Evaluate the Activity and Safety of Inebilizumab in Anti-Nmda Receptor Encephalitis and Assess Markers of Disease
Who cites it
70 citing papers in PubMed, 124 citations in OpenAlex.
- Daratumumab Treatment in Severe Anti-NMDAR Encephalitis: Two Case Reports and Literature Review.Neurology(R) neuroimmunology & neuroinflammation · 2026Review
- Effectiveness and safety of efgartigimod in patients with anti-NMDAR or anti-LGI1 encephalitis and itsNeuroprotection (Chichester, England) · 2026Article
- Anti-NMDA Receptor Encephalitis Associated with Ovarian Teratoma: A Comprehensive Review.Biomedicines · 2026Review
- Antibody-Mediated Mechanisms in Autoimmune Neurological Disorders.The European journal of neuroscience · 2026Review
- Systemic and organ-specific autoantibodies and worse outcomes in autoimmune encephalitis: a multicenter cohort study.Frontiers in immunology · 2026Observational
- Immunopathological mechanisms in autoimmune encephalitis: from pathogenesis to targeted therapies.Frontiers in immunology · 2026Review
- Autoimmune encephalitis.Nature reviews. Disease primers · 2025Review
- Successful treatment with efgartigimod as an add-on therapy for acute attack of anti-NMDA receptor encephalitis: a case report.BMC neurology · 2025Article
- Immunoregulatory programs in anti-N-methyl-D-aspartate receptor encephalitis identified by single-cell multi-omics analysis.Clinical and translational medicine · 2025Article
- Antibodies in neurological diseases: Established, emerging, explorative.Immunological reviews · 2024Review
- [(Auto)immunity in focal epilepsy: mechanisms of (auto‑)immune-inflammatory epileptogenic neurodegeneration].Der Nervenarzt · 2024Review
- A precision counterstrike on central nervous system autoimmunity.Cell research · 2024Article
- Social stress induces autoimmune responses against the brain.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Autoimmune receptor encephalitis in ApoEMolecular medicine reports · 2023Article
- VH2+ Antigen-Experienced B Cells in the Cerebrospinal Fluid Are Expanded and Enriched in Pediatric Anti-NMDA Receptor Encephalitis.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Anti-NMDA and Anti-AMPA Receptor Antibodies in Central Disorders: Preclinical Approaches to Assess Their Pathological Role and Translatability to Clinic.International journal of molecular sciences · 2023Review
- Repositioning synthetic glucocorticoids in psychiatric disease associated with neural autoantibodies: a narrative review.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Transfer of patient's peripheral blood mononuclear cells (PBMCs) disrupts blood-brain barrier and induces anti-NMDAR encephalitis: a study of novel humanized PBMC mouse model.Journal of neuroinflammation · 2023Article
- The imbalance between Bregs, Tfh, and Tregs in patients with anti-N-methyl-D-aspartate receptor encephalitis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Antibodies Against Glutamic Acid Decarboxylase 65 Are Locally Produced in the CSF and Arise During Affinity Maturation.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
30 authors at 9 institutions in 3 countries.
Funding
Abstract
Objective: Autoimmune encephalitis is most frequently associated with anti-NMDAR autoantibodies. Their pathogenic relevance has been suggested by passive transfer of patients' cerebrospinal fluid (CSF) in mice in vivo. We aimed to analyze the intrathecal plasma cell repertoire, identify autoantibody-producing clones, and characterize their antibody signatures in recombinant form. Methods: Patients with recent onset typical anti-NMDAR encephalitis were subjected to flow cytometry analysis of the peripheral and intrathecal immune response before, during, and after immunotherapy. Recombinant human monoclonal antibodies (rhuMab) were cloned and expressed from matching immunoglobulin heavy- (IgH) and light-chain (IgL) amplicons of clonally expanded intrathecal plasma cells (cePc) and tested for their pathogenic relevance. Results: Intrathecal accumulation of B and plasma cells corresponded to the clinical course. The presence of cePc with hypermutated antigen receptors indicated an antigen-driven intrathecal immune response. Consistently, a single recombinant human GluN1-specific monoclonal antibody, rebuilt from intrathecal cePc, was sufficient to reproduce NMDAR epitope specificity in vitro. After intraventricular infusion in mice, it accumulated in the hippocampus, decreased synaptic NMDAR density, and caused severe reversible memory impairment, a key pathogenic feature of the human disease, in vivo. Interpretation: A CNS-specific humoral immune response is present in anti-NMDAR encephalitis specifically targeting the GluN1 subunit of the NMDAR. Using reverse genetics, we recovered the typical intrathecal antibody signature in recombinant form, and proved its pathogenic relevance by passive transfer of disease symptoms from man to mouse, providing the critical link between intrathecal immune response and the pathogenesis of anti-NMDAR encephalitis as a humorally mediated autoimmune disease.
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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.