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@ARTICLE{Gardyan:126568,
      author       = {A. Gardyan$^*$ and W. Osen$^*$ and I. Zörnig$^*$ and L.
                      Podola$^*$ and M. Agarwal$^*$ and S. Aulmann and E.
                      Ruggiero$^*$ and M. Schmidt$^*$ and N. Halama$^*$ and B.
                      Leuchs$^*$ and C. von Kalle$^*$ and P. Beckhove$^*$ and A.
                      Schneeweiss and D. Jäger$^*$ and S. Eichmüller$^*$},
      title        = {{I}dentification of {NY}-{BR}-1-specific {CD}4(+) {T} cell
                      epitopes using {HLA}-transgenic mice.},
      journal      = {International journal of cancer},
      volume       = {136},
      number       = {11},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2017-02596},
      pages        = {2588 - 2597},
      year         = {2015},
      abstract     = {Breast cancer represents the second most common cancer type
                      worldwide and has remained the leading cause of
                      cancer-related deaths among women. The differentiation
                      antigen NY-BR-1 appears overexpressed in invasive mammary
                      carcinomas compared to healthy breast tissue, thus
                      representing a promising target antigen for T cell based
                      tumor immunotherapy approaches. Since efficient immune
                      attack of tumors depends on the activity of tumor
                      antigen-specific CD4(+) effector T cells, NY-BR-1 was
                      screened for the presence of HLA-restricted CD4(+) T cell
                      epitopes that could be included in immunological treatment
                      approaches. Upon NY-BR-1-specific DNA immunization of
                      HLA-transgenic mice and functional ex vivo analysis, a panel
                      of NY-BR-1-derived library peptides was determined that
                      specifically stimulated IFNγ secretion among splenocytes of
                      immunized mice. Following in silico analyses, four candidate
                      epitopes were determined which were successfully used for
                      peptide immunization to establish NY-BR-1-specific,
                      HLA-DRB1*0301- or HLA-DRB1*0401-restricted CD4(+) T cell
                      lines from splenocytes of peptide immunized HLA-transgenic
                      mice. Notably, all four CD4(+) T cell lines recognized human
                      HLA-DR-matched dendritic cells (DC) pulsed with lysates of
                      NY-BR-1 expressing human tumor cells, demonstrating natural
                      processing of these epitopes also within the human system.
                      Finally, CD4(+) T cells specific for all four CD4(+) T cell
                      epitopes were detectable among PBMC of breast cancer
                      patients, showing that CD4(+) T cell responses against the
                      new epitopes are not deleted nor inactivated by
                      self-tolerance mechanisms. Our results present the first
                      NY-BR-1-specific HLA-DRB1*0301- and HLA-DRB1*0401-restricted
                      T cell epitopes that could be exploited for therapeutic
                      intervention against breast cancer.},
      keywords     = {Antigens, Neoplasm (NLM Chemicals) / Epitopes, T-Lymphocyte
                      (NLM Chemicals) / HLA-DRB1 Chains (NLM Chemicals) /
                      HLA-DRB1*03:01 antigen (NLM Chemicals) / HLA-DRB1*04:01
                      antigen (NLM Chemicals) / Peptide Library (NLM Chemicals) /
                      breast cancer antigen NY-BR-1, human (NLM Chemicals) /
                      Interferon-gamma (NLM Chemicals)},
      cin          = {D015 / D120 / G100 / F010 / G010 / G183 / G182},
      ddc          = {610},
      cid          = {I:(DE-He78)D015-20160331 / I:(DE-He78)D120-20160331 /
                      I:(DE-He78)G100-20160331 / I:(DE-He78)F010-20160331 /
                      I:(DE-He78)G010-20160331 / I:(DE-He78)G183-20160331 /
                      I:(DE-He78)G182-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25387692},
      doi          = {10.1002/ijc.29322},
      url          = {https://inrepo02.dkfz.de/record/126568},
}