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@ARTICLE{Reincke:285128,
      author       = {S. M. Reincke and N. von Wardenburg and M. A. Homeyer and
                      H.-C. Kornau and G. Spagni and L. Y. Li and J. Kreye and E.
                      Sánchez-Sendín and S. Blumenau and D. Stappert and H.
                      Radbruch and A. E. Hauser and A. Künkele$^*$ and I. Edes
                      and D. Schmitz and H. Prüss},
      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     = {DKFZ-2023-02252},
      pages        = {5084-5097.e18},
      year         = {2023},
      note         = {2023 Nov 9;186(23):5084-5097.e18},
      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     = {CAAR T cell (Other) / NMDA receptor encephalitis (Other) /
                      T cells (Other) / autoimmune encephalitis (Other) /
                      autoimmunity (Other) / cell therapy (Other) / chimeric
                      autoantibody receptor (Other)},
      cin          = {BE01},
      ddc          = {610},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37918394},
      doi          = {10.1016/j.cell.2023.10.001},
      url          = {https://inrepo02.dkfz.de/record/285128},
}