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@ARTICLE{Peighambari:301885,
      author       = {A. Peighambari and H. Huang and P. Metzger and M. Adlesic
                      and K. Zodel and S. Schäfer and P. Seidel and L. M. Braun
                      and J. Hülsdünker and W. Melchinger and M. Follo and M. Ku
                      and S. Haug and Y. Li and A. Köttgen and C. Schell and D.
                      von Elverfeldt and W. Reichardt and R. Zeiser$^*$ and M.
                      Heikenwalder$^*$ and R. Höfflin and M. Börries$^*$ and I.
                      J. Frew$^*$},
      title        = {{C}haracterisation of an autochthonous mouse cc{RCC} model
                      of immune checkpoint inhibitor therapy resistance.},
      journal      = {Scientific reports},
      volume       = {15},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01164},
      pages        = {19818},
      year         = {2025},
      abstract     = {Many metastatic clear cell renal cell carcinomas (ccRCC)
                      are resistant to immune checkpoint inhibitor therapies,
                      however the mechanisms underlying sensitivity or resistance
                      remain incompletely characterised. We demonstrate that
                      ccRCCs in the Vhl/Trp53/Rb1 mutant mouse model are resistant
                      to combined anti-PD-1/anti-CTLA-4 therapy alone and in
                      combination with additional therapeutic agents that reflect
                      current ccRCC clinical trials. However, in some animals in
                      vivo checkpoint therapy allowed isolated splenic T cells to
                      recognise cultured ccRCC cells from the same animal,
                      implicating the tumour microenvironment in suppression of T
                      cell activation. We identified putative immunosuppressive
                      myeloid cell populations with features similar to myeloid
                      cells in the microenvironment of human ccRCC. The expression
                      patterns of immune checkpoint ligands in both the mouse
                      model and in human ccRCC suggests that several checkpoint
                      systems other than PD-1 and CTLA-4 are likely to represent
                      the dominant T cell suppressive forces in ccRCC. Our
                      findings characterise an autochthonous mouse ccRCC model of
                      immune checkpoint inhibitor therapy resistance and pave the
                      way for a systematic functional dissection of the identified
                      potential molecular barriers to effective immune therapy of
                      ccRCC.},
      keywords     = {Animals / Immune Checkpoint Inhibitors: pharmacology /
                      Immune Checkpoint Inhibitors: therapeutic use / Carcinoma,
                      Renal Cell: drug therapy / Carcinoma, Renal Cell: pathology
                      / Carcinoma, Renal Cell: immunology / Carcinoma, Renal Cell:
                      genetics / Mice / Kidney Neoplasms: drug therapy / Kidney
                      Neoplasms: pathology / Kidney Neoplasms: immunology / Kidney
                      Neoplasms: genetics / Disease Models, Animal / Drug
                      Resistance, Neoplasm / Humans / Tumor Microenvironment: drug
                      effects / Tumor Microenvironment: immunology / CTLA-4
                      Antigen: antagonists $\&$ inhibitors / T-Lymphocytes:
                      immunology / Programmed Cell Death 1 Receptor: antagonists
                      $\&$ inhibitors / Cell Line, Tumor / Immune Checkpoint
                      Inhibitors (NLM Chemicals) / CTLA-4 Antigen (NLM Chemicals)
                      / Programmed Cell Death 1 Receptor (NLM Chemicals)},
      cin          = {FR01 / D440},
      ddc          = {600},
      cid          = {I:(DE-He78)FR01-20160331 / I:(DE-He78)D440-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40473819},
      doi          = {10.1038/s41598-025-04917-1},
      url          = {https://inrepo02.dkfz.de/record/301885},
}