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Human neurexin-3α antibodies associate with encephalitis and alter synapse development
Nuria Gresa-Arribas1, Jesús Planagumà1, Mar Petit-Pedrol1
1From the Neuroimmunology Program, Biomedical Research Institute August Pi i Sunyer (IDIBAPS) (N.G.-A., J.P., M.P.-P., T.A., E.M.-H., F.G., J.D.), and Service of Neurology, Hospital Clínic (F.G.), University of Barcelona, Spain; Department of Neurology (I.K., S.K.), Brain Research Institute, Niigata University, Japan; Division of Pediatric Infectious Diseases (C.A.G.), Kaiser Permanente, Oakland Medical Center and University of California, San Francisco; Neurology Division (M.M.S.), Hospital das Clínicas, São Paulo University (HC/FMUSP), Brazil; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital; Department of Neurology (J.D.), University of Pennsylvania, Philadelphia; and Catalan Institution for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. N.G.-A. is currently affiliated with the Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.
This study identifies neurexin-3α autoantibodies as a cause of severe autoimmune encephalitis. These antibodies disrupt synapse development, suggesting a potential new therapeutic target for this neurological disorder.
Area of Science:
- Neuroimmunology
- Neurology
- Cell Biology
Background:
- Autoimmune encephalitis is a group of severe neurological disorders.
- Identifying specific autoantigens is crucial for diagnosis and treatment.
Purpose of the Study:
- To identify the autoantigen targeted by antibodies in a novel autoimmune encephalitis.
- To characterize the clinical presentation and outcomes of patients with this encephalitis.
- To investigate the pathogenic mechanism of the identified autoantibodies.
Main Methods:
- Patient serum analysis using immunoprecipitation and cell-based assays.
- Clinical data collection and neurological examination.
- In vitro studies on cultured neurons exposed to patient antibodies.
Main Results:
- Neurexin-3α was identified as the autoantigen in five patients with encephalitis.
- Patients presented with fever, confusion, seizures, and altered consciousness, with some developing dyskinesias or requiring respiratory support.
- In vitro, patient IgG decreased neurexin-3α clusters and synapse numbers in developing neurons but not mature ones.
Conclusions:
- Neurexin-3α autoantibodies are associated with a severe autoimmune encephalitis.
- The antibodies impair synapse development, indicating a potential mechanism for the observed neurological deficits.
- This finding suggests neurexin-3α autoantibodies may represent a treatable form of encephalitis.
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