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@ARTICLE{Kropp:284800,
      author       = {K. N. Kropp$^*$ and M. Fatho$^*$ and E. Huduti$^*$ and M.
                      Faust$^*$ and S. Lübcke$^*$ and V. Lennerz$^*$ and A.
                      Paschen$^*$ and M. Theobald$^*$ and T. Wölfel$^*$ and C.
                      Wölfel$^*$},
      title        = {{T}argeting the melanoma-associated antigen {CSPG}4 with
                      {HLA}-{C}*07:01-restricted {T}-cell receptors.},
      journal      = {Frontiers in immunology},
      volume       = {14},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DKFZ-2023-02103},
      pages        = {1245559},
      year         = {2023},
      abstract     = {Chondroitin sulfate proteoglycan 4 (CSPG4), also known as
                      high molecular weight-melanoma associated antigen, is
                      expressed in melanoma but also other tumor entities and
                      constitutes an attractive target for immunotherapeutic
                      approaches. While recent preclinical reports focused on
                      anti-CSPG4 chimeric antigen receptors (CAR), we here explore
                      T-cell receptor (TCR)-based approaches targeting CSPG4.The
                      TCRs of two CSPG4-reactive T-cell clones (11C/73 and 2C/165)
                      restricted by the highly prevalent HLA-C*07:01 allele were
                      isolated and the respective αβTCR pairs were retrovirally
                      expressed in CRISPR/Cas9-edited TCR-knockout T cells for
                      functional testing. We also combined alpha and beta TCR
                      chains derived from 11C/73 and 2C/165 in a cross-over
                      fashion to assess for hemichain dominance. CSPG4+ melanoma,
                      glioblastoma and lung cancer cell lines were identified and,
                      if negative, retrovirally transduced with
                      HLA-C*07:01.Functional tests confirmed specific recognition
                      of CSPG4+HLA-C*07:01+ target cells by the αβTCR retrieved
                      from the parental T-cell clones and in part also by the
                      cross-over TCR construct 2Cα-11Cβ. Despite high surface
                      expression, the 11Cα-2Cβ combination, however, was not
                      functional.Collectively, 11C/73- and 2C/165-expressing T
                      cells specifically and efficiently recognized
                      CSPG4+HLA-C*07:01+ cancer cells which warrants further
                      preclinical and clinical evaluation of these TCRs.},
      keywords     = {CSPG4 (Other) / T cell receptor (TCR) (Other) / TCR
                      hemichain dominance (Other) / chondroitin sulfate
                      proteoglycan 4 (Other) / tumor immunotherapy (Other)},
      cin          = {FM01 / ED01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331 / I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37849763},
      pmc          = {pmc:PMC10577170},
      doi          = {10.3389/fimmu.2023.1245559},
      url          = {https://inrepo02.dkfz.de/record/284800},
}