ArticleNature communications2020
Lupus autoantibodies act as positive allosteric modulators at GluN2A-containing NMDA receptors and impair spatial memory.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Neuropsychiatric systemic lupus erythematosus - current and novel treatments.Current opinion in rheumatology · 2026Review
- Cryo-EM of autoantibody-bound NMDA receptors reveals antigenic hotspots in an active immunization model of anti-NMDAR encephalitis.Science advances · 2026Article
- Novel binding mode for negative allosteric NMDA receptor modulators.The Journal of general physiology · 2026Article
- Neurotransmitters as regulators of autoimmunity: mechanisms and translational targeting.NPJ autoimmunity · 2026Review
- Diffuse neuropsychiatric lupus: Clinical evidence, immune-mediated mechanisms, and therapeutic insights.Seminars in immunology · 2025Review
- Spatiotemporal terahertz modulation enhances NMDAR-mediated miniature EPSCs.Scientific reports · 2025Article
- Review
- Structural basis for antibody-mediated NMDA receptor clustering and endocytosis in autoimmune encephalitis.Nature structural & molecular biology · 2024Article
- Recent advances in the diagnosis and management of neuropsychiatric lupus.Nature reviews. Rheumatology · 2024Review
- Human-derived monoclonal autoantibodies as interrogators of cellular proteotypes in the brain.Trends in neurosciences · 2024Review
- Correlation between neuropsychiatric systemic lupus erythematosus and immunological markers: a real-world retrospective study.Clinical rheumatology · 2024Article
- Novel α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR) potentiator LT-102: A promising therapeutic agent for treating cognitive impairment associated with schizophrenia.CNS neuroscience & therapeutics · 2024Article
- Lupus autoantibodies initiate neuroinflammation sustained by continuous HMGB1:RAGE signaling and reversed by increased LAIR-1 expression.Nature immunology · 2024Article
- Structural insights into NMDA receptor pharmacology.Biochemical Society transactions · 2023Review
- Disturbance of neuron-microglia crosstalk mediated by GRP78 in Neuropsychiatric systemic lupus erythematosus mice.Journal of neuroinflammation · 2023Article
- Progresses in GluN2A-containing NMDA Receptors and their Selective Regulators.Cellular and molecular neurobiology · 2023Review
- Mouse models, antibodies, and neuroimaging: Current knowledge and future perspectives in neuropsychiatric systemic lupus erythematosus (NPSLE).Frontiers in psychiatry · 2023Review
- NMDAR1 autoantibodies amplify behavioral phenotypes of genetic white matter inflammation: a mild encephalitis model with neuropsychiatric relevance.Molecular psychiatry · 2022Article
- Autoantibodies in Neuropsychiatric Systemic Lupus Erythematosus (NPSLE): Can They Be Used as Biomarkers for the Differential Diagnosis of This Disease?Clinical reviews in allergy & immunology · 2022Review
- Development and characterization of functional antibodies targeting NMDA receptors.Nature communications · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Patients with Systemic lupus erythematosus (SLE) experience various peripheral and central nervous system manifestations including spatial memory impairment. A subset of autoantibodies (DNRAbs) cross-react with the GluN2A and GluN2B subunits of the NMDA receptor (NMDAR). We find that these DNRAbs act as positive allosteric modulators on NMDARs with GluN2A-containing NMDARs, even those containing a single GluN2A subunit, exhibiting a much greater sensitivity to DNRAbs than those with exclusively GluN2B. Accordingly, GluN2A-specific antagonists provide greater protection from DNRAb-mediated neuronal cell death than GluN2B antagonists. Using transgenic mice to perturb expression of either GluN2A or GluN2B in vivo, we find that DNRAb-mediated disruption of spatial memory characterized by early neuronal cell death and subsequent microglia-dependent pathologies requires GluN2A-containing NMDARs. Our results indicate that GluN2A-specific antagonists or negative allosteric modulators are strong candidates to treat SLE patients with nervous system dysfunction.
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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.