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@ARTICLE{Wenke:140669,
      author       = {Wenke, Nina Kerstin and Kreye, Jakob and Andrzejak, Ewa and
                      Casteren, Adriana and Leubner, Jonas and Murgueitio, Manuela
                      S and Reincke, S Momsen and Secker, Christopher and Schmidl,
                      Lars and Geis, Christian and Ackermann, Frauke and Nikolaus,
                      Marc and Garner, Craig C and Wardemann, Hedda and Wolber,
                      Gerhard and Prüss, Harald},
      title        = {{N}-methyl-{D}-aspartate receptor dysfunction by unmutated
                      human antibodies against the {NR}1 subunit.},
      journal      = {Annals of neurology},
      volume       = {85},
      number       = {5},
      issn         = {0364-5134},
      address      = {Hoboken, NJ},
      publisher    = {Wiley-Blackwell},
      reportid     = {DZNE-2020-06991},
      pages        = {771-776},
      year         = {2019},
      abstract     = {Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is
                      the most common autoimmune encephalitis related to
                      autoantibody-mediated synaptic dysfunction. Cerebrospinal
                      fluid-derived human monoclonal NR1 autoantibodies showed low
                      numbers of somatic hypermutations or were unmutated. These
                      unexpected germline-configured antibodies showed weaker
                      binding to the NMDAR than matured antibodies from the same
                      patient. In primary hippocampal neurons, germline NR1
                      autoantibodies strongly and specifically reduced total and
                      synaptic NMDAR currents in a dose- and time-dependent
                      manner. The findings suggest that functional NMDAR
                      antibodies are part of the human naïve B cell repertoire.
                      Given their effects on synaptic function, they might
                      contribute to a broad spectrum of neuropsychiatric symptoms.
                      Ann Neurol 2019;85:771-776.},
      keywords     = {Animals / Anti-N-Methyl-D-Aspartate Receptor Encephalitis:
                      blood / Anti-N-Methyl-D-Aspartate Receptor Encephalitis:
                      pathology / Autoantibodies: blood / HEK293 Cells /
                      Hippocampus: chemistry / Hippocampus: metabolism /
                      Hippocampus: pathology / Humans / Mice / Neurons: chemistry
                      / Neurons: metabolism / Protein Binding: physiology /
                      Protein Structure, Secondary / Receptors,
                      N-Methyl-D-Aspartate: blood / Receptors,
                      N-Methyl-D-Aspartate: chemistry},
      cin          = {AG Prüß / AG Garner / AG Ackermann},
      ddc          = {610},
      cid          = {I:(DE-2719)1810003 / I:(DE-2719)1810001 /
                      I:(DE-2719)1813004},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 341
                      - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30843274},
      pmc          = {pmc:PMC6593665},
      doi          = {10.1002/ana.25460},
      url          = {https://pub.dzne.de/record/140669},
}