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@ARTICLE{Denk:299511,
      author       = {D. Denk and M. Ramakrishnan and C. Conche and C. Pallangyo
                      and M. Pesic and F. Ceteci and K. B. Kennel and A. C.
                      Kirisözü and E. Engel and K. Mohs and B. Ritter and A. M.
                      Pardo and E. Özkurt and F. Hildebrand and A. Waisman and M.
                      C. Arkan$^*$ and F. R. Greten$^*$},
      title        = {{IL}-17{RA} signaling provides dual tumor-suppressor
                      function during late-stage colorectal carcinogenesis.},
      journal      = {Immunity},
      volume       = {58},
      number       = {3},
      issn         = {1074-7613},
      address      = {[Cambridge, Mass.]},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2025-00469},
      pages        = {701-715.e8},
      year         = {2025},
      note         = {2025 Mar 11;58(3):701-715.e8},
      abstract     = {Expression of interleukin (IL)-17 family cytokines is
                      associated with tumor-promoting inflammation. We found that
                      low expression of IL17RA associated with worse prognosis in
                      late-stage colorectal cancer (CRC) patients. Deletion of
                      Il17ra in intestinal epithelial cells (IECs) in a murine
                      model of CRC enhanced epithelial-to-mesenchymal transition
                      (EMT) via increased expression of the epidermal growth
                      factor receptor and subsequent activation of the kinase Src.
                      Yet, these mice were protected from metastatic disease;
                      Il17ra deletion impaired intestinal barrier function and
                      enhanced systemic fungal invasion and associated immunity.
                      However, in macrophages, IL-17RA was required for spleen
                      tyrosine kinase (Syk) activation upon fungal-induced
                      dectin-1 engagement, and Il17ra ablation impaired IL-18
                      release and protective CD8+ T cell-mediated anti-tumor
                      immunity. Combining recombinant IL-17 and heat-killed
                      Candida albicans rendered colorectal tumors sensitive to
                      α-PD-1 treatment in a model of microsatellite stable (MSS)
                      CRC. Thus, IL-17RA engages two distinct tumor-suppressive
                      mechanisms in CRC, linking EMT and fungal-induced anti-tumor
                      immunity during tumor progression.},
      keywords     = {CRC (Other) / EMT (Other) / IL-17 (Other) / IL-17RA (Other)
                      / anti-tumor immunity (Other) / colon cancer (Other) /
                      immunotherapy (Other) / inflammation (Other) / mycobiome
                      (Other)},
      cin          = {FM01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40023157},
      doi          = {10.1016/j.immuni.2025.02.005},
      url          = {https://inrepo02.dkfz.de/record/299511},
}