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@ARTICLE{vanCasteren:165620,
      author       = {van Casteren, Adriana C M and Ackermann, Frauke and Rahman,
                      Kazi Atikur and Andrzejak, Ewa and Rosenmund, Christian and
                      Kreye, Jakob and Prüss, Harald and Garner, Craig Curtis and
                      Ichkova, Aleksandra},
      title        = {{D}ifferential modes of action of α1- and α1γ2-
                      autoantibodies derived from patients with {GABAAR}
                      encephalitis.},
      journal      = {eNeuro},
      volume       = {9},
      number       = {6},
      issn         = {2373-2822},
      address      = {Washington, DC},
      publisher    = {Soc.},
      reportid     = {DZNE-2022-01753},
      pages        = {ENEURO.0369-22.2022},
      year         = {2022},
      abstract     = {Autoantibodies against central nervous system proteins are
                      increasingly being recognized in association with neurologic
                      disorders. Although a growing number of neural
                      autoantibodies have been identified, a causal link between
                      specific autoantibodies and disease symptoms remains
                      unclear, as most studies use patient-derived CSF-containing
                      mixtures of autoantibodies. This raises questions concerning
                      mechanism of action and which autoantibodies truly
                      contribute to disease progression. To address this issue,
                      monoclonal autoantibodies were isolated from a young girl
                      with a range of neurologic symptoms, some of which reacted
                      with specific GABAA receptor (GABAAR) subunits, α1-subunit
                      and α1γ2-subunit, which in this study we have
                      characterized in detail using a combination of cellular
                      imaging and electrophysiological techniques. These studies
                      in neurons from wild-type mice (C57BL/6J;
                      $RRID:IMSR_JAX:000664)$ of mixed-sex revealed that the α1
                      and α1γ2 subunit-specific antibodies have differential
                      effects on the GABAA receptor. Namely, the α1-antibody was
                      found to directly affect GABAA receptor function on a short
                      time scale that diminished GABA currents, leading to
                      increased network excitability. On longer time scales those
                      antibodies also triggered a redistribution of the GABAA
                      receptor away from synapses. In contrast, the
                      α1γ2-antibody had no direct effect on GABAA receptor
                      function and could possibly mediate its effect through other
                      actors of the immune system. Taken together, these data
                      highlight the complexity underlying autoimmune disorders and
                      show that antibodies can exert their effect through many
                      mechanisms within the same disease.},
      keywords     = {Animals / Mice / Receptors, GABA-A: metabolism /
                      Autoantibodies: metabolism / Mice, Inbred C57BL /
                      Encephalitis / gamma-Aminobutyric Acid / Receptors, GABA-A
                      (NLM Chemicals) / GABAAR (Other) / autoantibodies (Other) /
                      autoimmune encephalitis (Other) / cortical/striatal neurons
                      (Other) / network excitability (Other) / Autoantibodies (NLM
                      Chemicals) / gamma-Aminobutyric Acid (NLM Chemicals)},
      cin          = {AG Garner / AG Prüß / AG Ackermann},
      ddc          = {610},
      cid          = {I:(DE-2719)1810001 / I:(DE-2719)1810003 /
                      I:(DE-2719)1813004},
      pnm          = {351 - Brain Function (POF4-351) / 353 - Clinical and Health
                      Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9765394},
      pubmed       = {pmid:36446572},
      doi          = {10.1523/ENEURO.0369-22.2022},
      url          = {https://pub.dzne.de/record/165620},
}