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@ARTICLE{Wang:307665,
      author       = {J. Wang and Y. Qiu and Z. Marti and F. Li and M. Wacker and
                      P. Oldrati and L. Mühlenbruch$^*$ and L. Jin and H. Zhang
                      and W. Xu and T. Li and B. Roschitzki and W. Faigle and Y.
                      Liu and J. T. Nguyen and J.-H. Lee and V. Haunerdinger and
                      M. Hauri-Hohl and F. Momburg and J. Bauer$^*$ and H.-G.
                      Rammensee$^*$ and M. Sospedra and R. Magliozzi and R.
                      Reynolds and J. Walz$^*$ and R. Martin},
      title        = {{EBV} infection and {HLA}-{DR}15 jointly drive multiple
                      sclerosis by myelin peptide presentation.},
      journal      = {Cell},
      volume       = {nn},
      issn         = {0092-8674},
      address      = {[Cambridge, Mass.]},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2026-00122},
      pages        = {nn},
      year         = {2026},
      note         = {epub},
      abstract     = {Epstein-Barr virus (EBV) is involved in causing and
                      probably also in perpetuating multiple sclerosis (MS). Among
                      several mechanisms of how EBV may contribute are
                      transcriptome alterations, including changes of antigen
                      processing and preferential presentation of both viral and
                      self-antigens. Here, we report that EBV reprograms the
                      transcriptome and immunopeptidome presented on the
                      MS-associated human leukocyte antigen (HLA)-DR15 molecules
                      of infected B cells. Identical myelin basic protein (MBP)
                      peptides were found to be presented on both EBV-infected B
                      cells and MS brain tissue but not primary B cells and thymic
                      tissue. Peripheral memory and cerebrospinal fluid
                      (CSF)-derived CD4+ T cells of HLA-DR15+ MS patients
                      responded to MBP peptides, MBP(78-90) and/or MBP(83-90), and
                      T cell clones raised with these peptides recognized all MBP
                      peptides ending at amino acid MBP90 in MS brain tissue. Our
                      study provides a new mechanistic link for how the
                      environmental and genetic risk factors, EBV infection and
                      HLA-DR15 haplotype, may contribute jointly to MS.},
      keywords     = {B cells (Other) / Epstein-Barr virus (Other) / autoreactive
                      CD4(+) T cells (Other) / brain tissue (Other) /
                      immunopeptidome (Other) / multiple sclerosis (Other) /
                      myelin basic protein peptide (Other) / thymic tissue
                      (Other)},
      cin          = {TU01},
      ddc          = {610},
      cid          = {I:(DE-He78)TU01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41534530},
      doi          = {10.1016/j.cell.2025.12.046},
      url          = {https://inrepo02.dkfz.de/record/307665},
}