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@ARTICLE{Schmid:281645,
      author       = {Schmid, Jonas and Alberti, Chiara and Power, Laura and
                      Nuñez, Nicolás G and De Feo, Donatella and Tyystjärvi,
                      Sofia and Kulsvehagen, Laila and Kreiner, Victor and Ayroza
                      Bleher, Ana Beatriz and Lipps, Patrick and Swinnen, Stijn
                      and Ingelfinger, Florian and Ulutekin, Can and Chaubet,
                      Camille and Unger, Susanne and Kreutmair, Stefanie and
                      Marignier, Romain and Korn, Thomas and Pröbstel,
                      Anne-Katrin and Liblau, Roland and Becher, Burkhard},
      title        = {{I}mmune signatures link myelin oligodendrocyte
                      glycoprotein antibody-associated disease to other
                      autoantibody-mediated conditions.},
      journal      = {Science translational medicine},
      volume       = {17},
      number       = {819},
      issn         = {1946-6234},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DZNE-2025-01163},
      pages        = {eadw0358},
      year         = {2025},
      abstract     = {Myelin oligodendrocyte glycoprotein antibody-associated
                      disease (MOGAD) is a recently defined neurological
                      autoimmune condition. The pathogenesis of the disease
                      remains poorly understood, and no specific therapies are
                      currently approved. Here, a comprehensive single-cell
                      immunophenotyping of peripheral blood mononuclear cells from
                      two independent cohorts of patients with MOGAD revealed
                      pronounced immune perturbations in MOGAD when compared with
                      healthy controls and patients with multiple sclerosis.
                      Patients with MOGAD displayed an expansion of CXCR5-CD21-
                      activated naïve and double-negative B cell subsets, a
                      feature shared with patients with systemic lupus
                      erythematosus. In addition, we observed altered Fc gamma
                      receptor expression in natural killer cells, monocytes, and
                      dendritic cells. Within the T cell compartment, CXCR3+CD4+
                      memory T cells were reduced in the circulation of patients
                      with MOGAD compared with healthy controls, and this result
                      was mirrored in a transgenic mouse model that showed
                      retention of these cells in the inflamed central nervous
                      system. Together, these results demonstrate profound
                      systemic immune cell alterations in MOGAD and contribute to
                      a better understanding of this distinct disease entity.},
      keywords     = {Myelin-Oligodendrocyte Glycoprotein: immunology / Humans /
                      Animals / Autoantibodies: immunology / Female / Mice / Male
                      / Adult / Middle Aged / Mice, Transgenic / Leukocytes,
                      Mononuclear: immunology / Immunophenotyping / Myelin
                      Oligodendrocyte Glycoprotein Antibody-Associated Disease /
                      Myelin-Oligodendrocyte Glycoprotein (NLM Chemicals) /
                      Autoantibodies (NLM Chemicals)},
      cin          = {AG Pröbstel},
      ddc          = {500},
      cid          = {I:(DE-2719)1013045},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41061045},
      doi          = {10.1126/scitranslmed.adw0358},
      url          = {https://pub.dzne.de/record/281645},
}