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@ARTICLE{Li:281825,
      author       = {Li, Lucie Y and Höltje, Markus and Rasmussen, Helle
                      Foverskov and Halle, Lennard and Mayrhofer, Marie and
                      Blüthner, Martin and Prüss, Harald},
      title        = {{B}inding of established antinuclear antibodies to neurons
                      depends on tissue fixation and underlying autoantigens.},
      journal      = {Frontiers in immunology},
      volume       = {16},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DZNE-2025-01206},
      pages        = {1674907},
      year         = {2025},
      abstract     = {Antinuclear antibodies (ANAs) are central biomarkers in
                      rheumatological conditions and can drive disease pathology.
                      Much less is known about the role of ANAs in neurological
                      symptoms, although a number of experimental studies have
                      demonstrated direct effects on neuronal function, for
                      example in neuropsychiatric lupus erythematosus. Moreover,
                      it is unclear whether the ANAs detected in HEp-2 cell-based
                      assays, the gold standard for ANA diagnostics, can also be
                      recognized in modern screening assays for anti-neuronal
                      autoimmunity, such as staining on rodent brain sections or
                      neuronal cultures. In this study, we therefore conducted a
                      comparative mapping of ANA-positive sera with
                      well-characterized HEp-2 patterns to central nervous system
                      (CNS) tissue, utilizing fixed and unfixed murine brain
                      sections and primary murine neurons. We screened 74
                      ANA-positive sera classified into 14 individual patterns and
                      combinations thereof. Majority of the samples reacted with
                      fixed primary neurons $(99\%,$ 73/74 sera), followed by
                      fixed brain sections $(93\%,$ 69/74), but much less to
                      unfixed mouse brain $(54\%,$ 40/74). While the PM/SCL- and
                      RPOI-positive sera showed no binding to unfixed brain
                      sections, the U1RNP (U1 nuclear ribonucleoprotein particle)
                      and FBLN (fibrillarin) ANAs reacted strongly across all
                      assays, indicating differences in antigen accessibility.
                      These findings suggest that the majority of ANAs can
                      interact with neural components, which may obscure the
                      detection of other anti-neuronal autoantibodies. The
                      foundational mapping of ANA binding in CNS tissue provided
                      here can also facilitate recognition of 'CNS-specific ANAs,'
                      which bind to neuronal autoantigens but not to HEp-2 cells.
                      Future studies should explore the association with certain
                      neurological manifestations and the role of ANAs in neuronal
                      pathology.},
      keywords     = {Animals / Neurons: immunology / Neurons: metabolism /
                      Antibodies, Antinuclear: immunology / Antibodies,
                      Antinuclear: metabolism / Mice / Autoantigens: immunology /
                      Humans / Tissue Fixation / Brain: immunology / Brain:
                      metabolism / Female / Male / ANA (Other) / HEp-2 (Other) /
                      anti-neuronal antibodies (Other) / autoimmunity (Other) /
                      immunofluorescence (Other) / Antibodies, Antinuclear (NLM
                      Chemicals) / Autoantigens (NLM Chemicals)},
      cin          = {AG Prüß},
      ddc          = {610},
      cid          = {I:(DE-2719)1810003},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41142797},
      pmc          = {pmc:PMC12549672},
      doi          = {10.3389/fimmu.2025.1674907},
      url          = {https://pub.dzne.de/record/281825},
}