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@ARTICLE{Kreye:162857,
      author       = {Kreye, Jakob and Wright, Sukhvir K and Casteren, Adriana
                      and Stöffler, Laura and Machule, Marie-Luise and Reincke,
                      Momsen and Nikolaus, Marc and Hoof, Scott and Sanchez
                      Sendin, Elisa and Homeyer, Marie Alice and Cordero Gomez,
                      Cesar and Kornau, Hans-Christian and Schmitz, Dietmar and
                      Kaindl, Angela M and Boehm-Sturm, Philipp and Mueller,
                      Susanne and Wilson, Max A and Upadhya, Manoj A and Dhangar,
                      Divya R and Greenhill, Stuart and Woodhall, Gavin and Turko,
                      Paul and Vida, Imre and Garner, Craig Curtis and Wickel,
                      Jonathan and Geis, Christian and Fukata, Yuko and Fukata,
                      Masaki and Prüß, Harald},
      title        = {{E}ncephalitis patient-derived monoclonal {GABAA} receptor
                      antibodies cause epileptic seizures.},
      journal      = {Journal of experimental medicine},
      volume       = {218},
      number       = {11},
      issn         = {0022-1007},
      address      = {New York, NY},
      publisher    = {Rockefeller Univ. Press},
      reportid     = {DZNE-2021-01512},
      pages        = {e20210012},
      year         = {2021},
      abstract     = {Autoantibodies targeting the GABAA receptor (GABAAR)
                      hallmark an autoimmune encephalitis presenting with frequent
                      seizures and psychomotor abnormalities. Their pathogenic
                      role is still not well-defined, given the common overlap
                      with further autoantibodies and the lack of patient-derived
                      mAbs. Five GABAAR mAbs from cerebrospinal fluid cells bound
                      to various epitopes involving the α1 and γ2 receptor
                      subunits, with variable binding strength and partial
                      competition. mAbs selectively reduced GABAergic currents in
                      neuronal cultures without causing receptor internalization.
                      Cerebroventricular infusion of GABAAR mAbs and Fab fragments
                      into rodents induced a severe phenotype with seizures and
                      increased mortality, reminiscent of encephalitis patients'
                      symptoms. Our results demonstrate direct pathogenicity of
                      autoantibodies on GABAARs independent of Fc-mediated
                      effector functions and provide an animal model for GABAAR
                      encephalitis. They further provide the scientific rationale
                      for clinical treatments using antibody depletion and can
                      serve as tools for the development of antibody-selective
                      immunotherapies.},
      keywords     = {Animals / Antibodies, Monoclonal: immunology /
                      Autoantibodies: immunology / Autoantigens: immunology /
                      Cells, Cultured / Encephalitis: immunology / Epilepsy:
                      immunology / HEK293 Cells / Hippocampus: immunology / Humans
                      / Mice / Neurons: immunology / Receptors, GABA-A: immunology
                      / Seizures: immunology},
      cin          = {AG Prüß / AG Garner / AG Schmitz},
      ddc          = {610},
      cid          = {I:(DE-2719)1810003 / I:(DE-2719)1810001 /
                      I:(DE-2719)1810004},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 351 -
                      Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34546336},
      pmc          = {pmc:PMC8480667},
      doi          = {10.1084/jem.20210012},
      url          = {https://pub.dzne.de/record/162857},
}