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@ARTICLE{Reincke:265939,
      author       = {Reincke, Momsen and von-Wardenburg, Niels-Oliver and
                      Homeyer, Marie Alice and Kornau, Hans-Christian and Spagni,
                      Gregorio and Li, Lucie Y and Kreye, Jakob and
                      Sánchez-Sendín, Elisa and Blumenau, Sonja and Stappert,
                      Dominik and Radbruch, Helena and Hauser, Anja E and
                      Künkele, Annette and Edes, Inan and Schmitz, Dietmar and
                      Prüss, Harald},
      title        = {{C}himeric autoantibody receptor {T} cells deplete {NMDA}
                      receptor-specific {B} cells.},
      journal      = {Cell},
      volume       = {186},
      number       = {23},
      issn         = {0092-8674},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2023-01062},
      pages        = {5084 - 5097.e18},
      year         = {2023},
      abstract     = {Anti-NMDA receptor (NMDAR) autoantibodies cause NMDAR
                      encephalitis, the most common autoimmune encephalitis,
                      leading to psychosis, seizures, and autonomic dysfunction.
                      Current treatments comprise broad immunosuppression or
                      non-selective antibody removal. We developed NMDAR-specific
                      chimeric autoantibody receptor (NMDAR-CAAR) T cells to
                      selectively eliminate anti-NMDAR B cells and disease-causing
                      autoantibodies. NMDAR-CAARs consist of an extracellular
                      multi-subunit NMDAR autoantigen fused to intracellular
                      4-1BB/CD3ζ domains. NMDAR-CAAR T cells recognize a large
                      panel of human patient-derived autoantibodies, release
                      effector molecules, proliferate, and selectively kill
                      antigen-specific target cell lines even in the presence of
                      high autoantibody concentrations. In a passive transfer
                      mouse model, NMDAR-CAAR T cells led to depletion of an
                      anti-NMDAR B cell line and sustained reduction of
                      autoantibody levels without notable off-target toxicity.
                      Treatment of patients may reduce side effects, prevent
                      relapses, and improve long-term prognosis. Our preclinical
                      work paves the way for CAAR T cell phase I/II trials in
                      NMDAR encephalitis and further autoantibody-mediated
                      diseases.},
      keywords     = {Animals / Humans / Mice / Autoantibodies: metabolism /
                      Encephalitis: metabolism / Encephalitis: therapy /
                      Receptors, N-Methyl-D-Aspartate / T-Lymphocytes / Autoimmune
                      Diseases / Disease Models, Animal / CAAR T cell (Other) /
                      CAAR T cell (Other) / CAAR T cell (Other) / CAAR T cell
                      (Other) / CAAR T cell (Other) / CAAR T cell (Other) / NMDA
                      receptor encephalitis (Other) / T cells (Other) / autoimmune
                      encephalitis (Other) / autoimmunity (Other) / cell therapy
                      (Other) / chimeric autoantibody receptor (Other) /
                      Autoantibodies (NLM Chemicals) / Receptors,
                      N-Methyl-D-Aspartate (NLM Chemicals)},
      cin          = {AG Prüß / LAT / AG Schmitz},
      ddc          = {610},
      cid          = {I:(DE-2719)1810003 / I:(DE-2719)1040190 /
                      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},
      experiment   = {EXP:(DE-2719)LAT-20190308},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37918394},
      doi          = {10.1016/j.cell.2023.10.001},
      url          = {https://pub.dzne.de/record/265939},
}