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@ARTICLE{Ho:276892,
      author       = {P. Ho and J. C. Melms and M. Rogava and C. J. Frangieh and
                      J. Poźniak and S. B. Shah and Z. Walsh and O. Kyrysyuk and
                      A. D. Amin and L. Caprio and B. T. Fullerton and R. K. Soni
                      and C. R. Ager and J. Biermann and Y. Wang and M.
                      Khosravi-Maharlooei and G. Zanetti and M. Mu and H. Fatima
                      and E. K. Moore and N. Vasan and S. F. Bakhoum and S. L.
                      Reiner and C. Bernatchez and M. Sykes and E. M. Mace and K.
                      W. Wucherpfennig and D. Schadendorf$^*$ and O. Bechter and
                      P. Shah and G. K. Schwartz and J.-C. Marine and B. Izar},
      title        = {{T}he {CD}58-{CD}2 axis is co-regulated with {PD}-{L}1 via
                      {CMTM}6 and shapes anti-tumor immunity.},
      journal      = {Cancer cell},
      volume       = {41},
      number       = {7},
      issn         = {1535-6108},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2023-01194},
      pages        = {1207-1221.e12},
      year         = {2023},
      note         = {2023 Jul 10;41(7):1207-1221.e12},
      abstract     = {The cell-autonomous balance of immune-inhibitory and
                      -stimulatory signals is a critical process in cancer immune
                      evasion. Using patient-derived co-cultures, humanized mouse
                      models, and single-cell RNA-sequencing of patient melanomas
                      biopsied before and on immune checkpoint blockade, we find
                      that intact cancer cell-intrinsic expression of CD58 and
                      ligation to CD2 is required for anti-tumor immunity and is
                      predictive of treatment response. Defects in this axis
                      promote immune evasion through diminished T cell activation,
                      impaired intratumoral T cell infiltration and proliferation,
                      and concurrently increased PD-L1 protein stabilization.
                      Through CRISPR-Cas9 and proteomics screens, we identify and
                      validate CMTM6 as critical for CD58 stability and
                      upregulation of PD-L1 upon CD58 loss. Competition between
                      CD58 and PD-L1 for CMTM6 binding determines their rate of
                      endosomal recycling over lysosomal degradation. Overall, we
                      describe an underappreciated yet critical axis of cancer
                      immunity and provide a molecular basis for how cancer cells
                      balance immune inhibitory and stimulatory cues.},
      keywords     = {CD2 (Other) / CD58 (Other) / CRISPR-Cas9 screen (Other) /
                      PDL1 (Other) / balance of co-inhibitory/co-stimulator
                      (Other) / cancer immune evasion (Other) / cancer immunology
                      (Other) / cancer immunotherapy (Other) / immune checkpoint
                      blockade (Other) / mass spec screen (Other) / resistance to
                      immune checkpoint blockade (Other) / single-cell
                      RNA-sequencing (Other)},
      cin          = {ED01},
      ddc          = {610},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37327789},
      doi          = {10.1016/j.ccell.2023.05.014},
      url          = {https://inrepo02.dkfz.de/record/276892},
}