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@ARTICLE{Schiele:301513,
      author       = {P. Schiele and A. S. Japp and R. Stark and J. J. Sattelberg
                      and C. Nikolaou and G. Kornhuber and P. Abbasi and N. Ding
                      and S. Rosnev and S. Meinke and K. Mühle and L. Loyal and
                      J. Braun and M. Dingeldey and S. Durlanik and N. Matzmohr
                      and D. Ponikwicka-Tyszko and S. Wolczynski and N. A. Rahman
                      and I. Taniuchi and S. Schlickeiser and C. Giesecke-Thiel
                      and T. Blankenstein and I.-K. Na$^*$ and A. Thiel and M.
                      Frentsch},
      title        = {{CD}8+ {T} cell-derived {CD}40{L} mediates noncanonical
                      cytotoxicity in {CD}40-expressing cancer cells.},
      journal      = {Science advances},
      volume       = {11},
      number       = {21},
      issn         = {2375-2548},
      address      = {Washington, DC [u.a.]},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2025-01050},
      pages        = {eadr9331},
      year         = {2025},
      abstract     = {T cells and their effector functions, in particular the
                      canonical cytotoxicity of CD8+ T cells involving perforin,
                      granzymes, Fas ligand (FasL), and tumor necrosis factor
                      related apoptosis inducing ligand (TRAIL), are crucial for
                      tumor immunity. Here, we reveal a previously unidentified
                      mechanism by which CD40L-expressing CD8+ T cells induce
                      cytotoxicity in cancer cells. In murine models, up to $50\%$
                      of tumor-specific CD8+ T cells expressed CD40L, and
                      conditional CD40L ablation in CD8+ T cells alone led to
                      tumor formation. Mechanistically, CD40L+CD8+ T cells can
                      induce cell death in CD40-expressing cancer cells by
                      triggering caspase-8 activation. We demonstrate that a gene
                      signature for resistance to CD40 signaling-induced cell
                      death strongly correlates with worse survival in different
                      human cancer cohorts. Our results introduce CD40L as a
                      rather counterintuitive, noncanonical cytotoxic factor that
                      complements the capabilities of CD8+ T cells to combat
                      cancers and has the potential to enhance the efficacy of
                      immunotherapies.},
      keywords     = {CD8-Positive T-Lymphocytes: immunology / CD8-Positive
                      T-Lymphocytes: metabolism / CD40 Ligand: metabolism / CD40
                      Ligand: genetics / CD40 Ligand: immunology / Animals /
                      Humans / CD40 Antigens: metabolism / CD40 Antigens: genetics
                      / Mice / Cell Line, Tumor / Neoplasms: immunology /
                      Neoplasms: metabolism / Neoplasms: pathology / Neoplasms:
                      genetics / Cytotoxicity, Immunologic / Signal Transduction /
                      Caspase 8: metabolism / CD40 Ligand (NLM Chemicals) / CD40
                      Antigens (NLM Chemicals) / Caspase 8 (NLM Chemicals)},
      cin          = {BE01},
      ddc          = {500},
      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:40397730},
      doi          = {10.1126/sciadv.adr9331},
      url          = {https://inrepo02.dkfz.de/record/301513},
}