ArticleNeurology(R) neuroimmunology & neuroinflammation2020
Intrathecal B-cell activation in LGI1 antibody encephalitis.
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Article in Neurology(R) neuroimmunology & neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23citing papers in PubMed
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23 citing papers in PubMed, 36 citations in OpenAlex.
- Plasma proteome in LGI-1 autoimmune encephalitis.Journal of neuroinflammation · 2026Article
- Psychiatric symptoms as clinical warning signals of adult anti-LGI-1 encephalitis: an observational cohort study.BMC psychiatry · 2026Observational
- Immunopathological mechanisms in autoimmune encephalitis: from pathogenesis to targeted therapies.Frontiers in immunology · 2026Review
- Case Report: Sequential FcRn blockade and B-cell depletion for treatment-refractory relapsing autoimmune encephalitis: a three-patient case series.Frontiers in immunology · 2026Article
- Clinical, Electroencephalogram and Imaging Characteristics of Patients With Anti-LGI1 Antibody Encephalitis: A Multicenter Cohort Study.CNS neuroscience & therapeutics · 2025Article
- Autoimmune encephalitis associated with anti-LGI1 antibody: a potential cause of neuropsychiatric systemic lupus erythematosus.Lupus science & medicine · 2025Article
- B-cell immune repertoire analysis of autoimmune neurological syndromes with anti-GAD65 antibodies.Frontiers in neurology · 2025Article
- Flow cytometry identifies changes in peripheral and intrathecal lymphocyte patterns in CNS autoimmune disorders and primary CNS malignancies.Journal of neuroinflammation · 2024Article
- Leucine-rich Glioma Inactivated 1 (LGI-1) Limbic Encephalitis Presenting with Psychotic Symptoms without Seizures: A Case Report with Five-year Follow-up and Review of Literature.Indian journal of psychological medicine · 2024Article
- Leucine-Rich Glioma-Inactivated 1 (LGI1) Protein Stimulates Proliferation and IL-10 Production in Peripheral Blood Mononuclear Cells of Patients with LGI1 Antibody-Mediated Autoimmune Encephalitis In Vitro.International journal of molecular sciences · 2024Article
- Ultrahigh frequencies of peripherally matured LGI1- and CASPR2-reactive B cells characterize the cerebrospinal fluid in autoimmune encephalitis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- HLA dependency and possible clinical relevance of intrathecally synthesized anti-IgLON5 IgG4 in anti-IgLON5 disease.Frontiers in immunology · 2024Article
- Leucine-rich Glioma-inactivated 1 Encephalitis Followed by Isaacs Syndrome: Alternating Presence of Pathogenic Autoantibodies to Leucine-rich Glioma-inactivated 1 and Contactin-associated Protein-like 2.Internal medicine (Tokyo, Japan) · 2023Article
- Circulating plasmablasts and follicular helper T-cell subsets are associated with antibody-positive autoimmune epilepsy.Frontiers in immunology · 2022Article
- Next Generation Sequencing of Cerebrospinal Fluid B Cell Repertoires in Multiple Sclerosis and Other Neuro-Inflammatory Diseases-A Comprehensive Review.Diagnostics (Basel, Switzerland) · 2021Review
- Clinical and Prognostic Value of Immunogenetic Characteristics in Anti-LGI1 Encephalitis.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
- Comprehensive B-Cell Immune Repertoire Analysis of Anti-NMDAR Encephalitis and Anti-LGI1 Encephalitis.Frontiers in immunology · 2021Article
- Positive LGI1 Antibodies in CSF and Relapse Relate to Worse Outcome in Anti-LGI1 Encephalitis.Frontiers in immunology · 2021Article
- Short- and Long-Lived Autoantibody-Secreting Cells in Autoimmune Neurological Disorders.Frontiers in immunology · 2021Review
- The B cell immunobiology that underlies CNS autoantibody-mediated diseases.Nature reviews. Neurology · 2020Review
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Authors and funding
14 authors at 1 institution in 2 countries.
Klaus Lehmann-HornFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK. klaus.lehmann-horn@tum.de.ORCID 0000-0001-5488-7549
Sarosh R IraniFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.ORCID 0000-0002-7667-9748
Shengzhi WangFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.
Arumugam PalanichamyFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.
Sarah JahnFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.
Ariele L GreenfieldFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.
Ravi DandekarFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.
Gildas LepennetierFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.ORCID 0000-0002-1899-3149
Sophia MichaelFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.ORCID 0000-0002-3342-7698
Jeffrey M GelfandFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.
Michael D GeschwindFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.
Michael R WilsonFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.ORCID 0000-0002-8705-5084
Scott S ZamvilFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.
H-Christian von BüdingenFrom the Department of Neurology (K.L.-H., S.W., A.P., S.J., A.L.G., R.D., J.M.G., M.D.G., M.R.W., S.S.Z., H.-C.v.B.), UCSF Weill Institute for Neurosciences; Program in Immunology (K.L.-H., S.S.Z.), UCSF, San Francisco, CA; Department of Neurology (K.L.-H., G.L.), Klinikum rechts der Isar, Technische Universität München, Germany; and Oxford Autoimmune Neurology Group (S.R.I., S.M.), John Radcliffe Hospital, University of Oxford, UK.
MACOM (United States) · US
Funding
Predicting progression of human prion diseaseR01AG031189 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GESCHWIND, MICHAEL D · 2008 to 2017
$5.7MRepertoire selection of AQP4-specific T cells that cause CNS autoimmunediseaseR01AI131624 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ZAMVIL, SCOTT S · 2019 to 2023
$2.2MDisease relevance of CD20 expression on T cells in multiple sclerosis patientsR01NS092835 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HAUSER, STEPHEN L · 2015 to 2018
$1.7MAntibody Mediated Autoimmunity in Neuromyelitis OpticaK02NS072288 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VON BUEDINGEN, HANS-CHRISTIAN · 2011 to 2015
$879kSingle cell RNA-Seq and clonal analysis of CD8+ T cells in MSR21AI142186 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ZAMVIL, SCOTT S · 2019 to 2020
$443kDepartment of HealthNIAID NIH HHS R01 AI131624NIAID NIH HHS R21 AI142186NIA NIH HHS R01 AG031189NINDS NIH HHS K02 NS072288NINDS NIH HHS R01 NS092835Wellcome TrustWellcome Trust 104079/Z/14/Z
Abstract
objectiveTo study intrathecal B-cell activity in leucine-rich, glioma-inactivated 1 (LGI1) antibody encephalitis. In patients with LGI1 antibodies, the lack of CSF lymphocytosis or oligoclonal bands and serum-predominant LGI1 antibodies suggests a peripherally initiated immune response. However, it is unknown whether B cells within the CNS contribute to the ongoing pathogenesis of LGI1 antibody encephalitis.
methodsPaired CSF and peripheral blood (PB) mononuclear cells were collected from 6 patients with LGI1 antibody encephalitis and 2 patients with other neurologic diseases. Deep B-cell immune repertoire sequencing was performed on immunoglobulin heavy chain transcripts from CSF B cells and sorted PB B-cell subsets. In addition, LGI1 antibody levels were determined in CSF and PB.
resultsSerum LGI1 antibody titers were on average 127-fold higher than CSF LGI1 antibody titers. Yet, deep B-cell repertoire analysis demonstrated a restricted CSF repertoire with frequent extensive clusters of clonally related B cells connected to mature PB B cells. These clusters showed intensive mutational activity of CSF B cells, providing strong evidence for an independent CNS-based antigen-driven response in patients with LGI1 antibody encephalitis but not in controls.
conclusionsOur results demonstrate that intrathecal immunoglobulin repertoire expansion is a feature of LGI1 antibody encephalitis and suggests a need for CNS-penetrant therapies.
Indexed as
B-LymphocytesAdultAgedAutoantibodiesEncephalitisFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMiddle AgedAutoantibodiesIntracellular Signaling Peptides and ProteinsLGI1 protein, human
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