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@ARTICLE{Aflalo:306260,
      author       = {A. Aflalo and A. F. Altenburg and M. Wacker and E. Khanfar
                      and J. Bauer$^*$ and J. S. Walz$^*$ and L. H. Boyle},
      title        = {{TAPBPR} promotes editing of the {HLA}-{B}44 peptide
                      repertoire, increasing the presentation of peptides
                      containing a {C}-terminal tryptophan.},
      journal      = {Frontiers in immunology},
      volume       = {16},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DKFZ-2025-02489},
      pages        = {1685705},
      year         = {2025},
      abstract     = {Major histocompatibility complex class I (MHC-I) molecules
                      play a key part in the adaptive immune response by
                      presenting antigens to CD8+ T cells. The high degree of
                      polymorphism in MHC-I leads to significant variation in
                      their dependence on the components of the antigen processing
                      and presentation pathway, such as the transporter associated
                      with antigen processing (TAP) and tapasin, and their
                      affinity for the peptide editor TAP-binding protein related
                      (TAPBPR). Here, we investigated the influence of TAPBPR on
                      the cell surface phenotype and peptide repertoire presented
                      by two human leukocyte antigen (HLA) class I allotypes,
                      HLA-B*44:02 and HLA-B*44:05, which are known to differ
                      drastically in their dependence on tapasin. TAPBPR bound
                      weakly to both HLA-B*44:02 and HLA-B*44:05. In contrast to
                      tapasin depletion, the loss of TAPBPR has a limited effect
                      on the cell surface expression of these two molecules.
                      Analysis of the immunopeptidomes presented in the presence
                      and absence of TAPBPR revealed that TAPBPR expression
                      restricted the peptide repertoire presented on HLA-B*44:05,
                      while it diversified the repertoire presented on
                      HLA-B*44:02. Overall, TAPBPR improved the predicted affinity
                      of the peptides displayed on both the HLA-B44 molecules.
                      Furthermore, TAPBPR enhanced the presentation of peptides
                      containing a C-terminal tryptophan residue. Our results show
                      that TAPBPR can significantly impact the peptide repertoire
                      of MHC-I molecules to which it binds weakly. Furthermore,
                      this represents the first study that points to a role for
                      TAPBPR in selecting a specific peptide sequence on MHC class
                      I molecules.},
      keywords     = {Humans / Antigen Presentation: immunology / HLA-B44
                      Antigen: immunology / HLA-B44 Antigen: metabolism / HLA-B44
                      Antigen: genetics / Tryptophan: immunology / Peptides:
                      immunology / Protein Binding / Membrane Transport Proteins /
                      CD8-Positive T-Lymphocytes: immunology / HLA (Other) / MHC
                      (Other) / TAPBPR (Other) / antigen presentation (Other) /
                      immunopeptidomics (Other) / HLA-B44 Antigen (NLM Chemicals)
                      / Tryptophan (NLM Chemicals) / Peptides (NLM Chemicals) /
                      tapasin (NLM Chemicals) / Membrane Transport Proteins (NLM
                      Chemicals)},
      cin          = {TU01},
      ddc          = {610},
      cid          = {I:(DE-He78)TU01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41246309},
      pmc          = {pmc:PMC12615179},
      doi          = {10.3389/fimmu.2025.1685705},
      url          = {https://inrepo02.dkfz.de/record/306260},
}