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@ARTICLE{Miao:285250,
      author       = {B. Miao$^*$ and Z. Hu$^*$ and R. Mezzadra and L.
                      Hoeijmakers and A. Fauster and S. Du$^*$ and Z. Yang and M.
                      Sator-Schmitt$^*$ and H. Engel$^*$ and X. Li and C.
                      Broderick and G. Jin and R. Gomez-Eerland and L. Rozeman and
                      X. Lei and H. Matsuo$^*$ and C. Yang$^*$ and I. Hofland and
                      D. Peters and A. Broeks and E. Laport$^*$ and A. Fitz$^*$
                      and X. Zhao$^*$ and M. A. A. Mahmoud$^*$ and X. Ma$^*$ and
                      S. Sander$^*$ and H.-K. Liu$^*$ and G. Cui$^*$ and Y. Gan
                      and W. Wu and Y. Xiao and A. J. R. Heck and W. Guan and S.
                      W. Lowe and H. M. Horlings and C. Wang and T. R. Brummelkamp
                      and C. U. Blank and T. N. M. Schumacher and C. Sun$^*$},
      title        = {{CMTM}6 shapes antitumor {T} cell response through
                      modulating protein expression of {CD}58 and {PD}-{L}1.},
      journal      = {Cancer cell},
      volume       = {41},
      number       = {10},
      issn         = {1535-6108},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2023-02285},
      pages        = {1817 - 1828.e9},
      year         = {2023},
      note         = {DKFZ-ZMBH Alliance / #EA:D250#LA:D250#},
      abstract     = {The dysregulated expression of immune checkpoint molecules
                      enables cancer cells to evade immune destruction. While
                      blockade of inhibitory immune checkpoints like PD-L1 forms
                      the basis of current cancer immunotherapies, a deficiency in
                      costimulatory signals can render these therapies futile.
                      CD58, a costimulatory ligand, plays a crucial role in
                      antitumor immune responses, but the mechanisms controlling
                      its expression remain unclear. Using two systematic
                      approaches, we reveal that CMTM6 positively regulates CD58
                      expression. Notably, CMTM6 interacts with both CD58 and
                      PD-L1, maintaining the expression of these two immune
                      checkpoint ligands with opposing functions. Functionally,
                      the presence of CMTM6 and CD58 on tumor cells significantly
                      affects T cell-tumor interactions and response to PD-L1-PD-1
                      blockade. Collectively, these findings provide fundamental
                      insights into CD58 regulation, uncover a shared regulator of
                      stimulatory and inhibitory immune checkpoints, and highlight
                      the importance of tumor-intrinsic CMTM6 and CD58 expression
                      in antitumor immune responses.},
      cin          = {D250 / A240 / D180 / D192},
      ddc          = {610},
      cid          = {I:(DE-He78)D250-20160331 / I:(DE-He78)A240-20160331 /
                      I:(DE-He78)D180-20160331 / I:(DE-He78)D192-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37683639},
      doi          = {10.1016/j.ccell.2023.08.008},
      url          = {https://inrepo02.dkfz.de/record/285250},
}