ArticleJournal of neuroinflammation2023
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.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- Stepwise Evolution of Immunodeficient Mouse Models: Focus on NCG Strains and Their Applications in Humanized Immune System Research.Vaccines · 2026Review
- Effectiveness and safety of efgartigimod in patients with anti-NMDAR or anti-LGI1 encephalitis and itsNeuroprotection (Chichester, England) · 2026Article
- Choroid Plexus Abnormalities in Autoimmune Encephalitis.CNS neuroscience & therapeutics · 2026Article
- Antibody-Mediated Mechanisms in Autoimmune Neurological Disorders.The European journal of neuroscience · 2026Review
- Phagocytic remodeling in CD74Translational cancer research · 2026Article
- Role of serum complement C3 in blood-brain barrier injury and prognosis of anti-NMDAR encephalitis.BMC neurology · 2026Article
- The immune-endothelial axis in neurovascular pathophysiology: a framework for targeted interventions.Frontiers in immunology · 2026Review
- Clinical and immunological correlates of elevated age-adjusted QAlb in anti-NMDAR encephalitis.Frontiers in human neuroscience · 2026Article
- Gut microbiota-neuroimmune crosstalk in autoimmune encephalitis: mechanistic insights and therapeutic prospects.Frontiers in microbiology · 2026Review
- Immunopathological mechanisms in autoimmune encephalitis: from pathogenesis to targeted therapies.Frontiers in immunology · 2026Review
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- NLRP3 Inflammasome Activation Contributes to Seizure Susceptibility in Anti-NMDAR Encephalitis: Evidence from Patients and a Mouse Model.Molecular neurobiology · 2025Article
- Endothelium glutamate receptors in brain pathology.Frontiers in pharmacology · 2025Review
- Progress in the preparation of an active immunization model of anti-N-methyl-D-aspartate receptor encephalitis in animals.Frontiers in immunology · 2025Review
- Immunoregulatory programs in anti-N-methyl-D-aspartate receptor encephalitis identified by single-cell multi-omics analysis.Clinical and translational medicine · 2025Article
- The P38MAPK Pathway Mediates the Destruction of the Blood-Brain Barrier in Anti-NMDAR Encephalitis Mice.Neurochemical research · 2024Article
- NMDA Receptors in Neurodevelopmental Disorders: Pathophysiology and Disease Models.International journal of molecular sciences · 2024Review
- The Involvement of Glial Cells in Blood-Brain Barrier Damage in Neuroimmune Diseases.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundAnti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe autoimmune neuropsychiatric disease. Brain access of anti-NMDAR autoantibody through the blood-brain barrier (BBB) is essential for pathogenesis. Most previous animal models limit the investigation of etiologies of BBB damage in patients.
methodsIn this study, we established a novel humanized mouse model of anti-NMDAR encephalitis by intraperitoneal injection of patients' peripheral blood mononuclear cells (PBMCs) into BALB/c Rag2
resultsWe found that engraftment of patients' PBMCs not only produced potent anti-GluN1 autoantibodies, but also disrupted BBB integrity to allow brain access of autoantibodies, resulting in a hyperactive locomotor phenotype, anxiety- and depressive-like behaviors, cognitive deficits, as well as functional changes in corresponding brain regions. Transcriptome analysis suggested an exaggerated immune response and impaired neurotransmission in the mouse model and highlighted Il-1β as a hub gene implicated in pathological changes. We further demonstrated that Il-1β was produced by endothelial cells and disrupted BBB by repressing tight junction proteins. Treatment with Anakinra, an Il-1 receptor antagonist, ameliorated BBB damage and neuropsychiatric behaviors.
conclusionsOur study provided a novel and clinically more relevant humanized mouse model of anti-NMDAR encephalitis and revealed an intrinsic pathogenic property of the patient's lymphocytes.
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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.