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@ARTICLE{McClanahan:258656,
      author       = {McClanahan, Fabienne and Riches, John C and Miller, Shaun
                      and Day, William P and Kotsiou, Eleni and Neuberg, Donna and
                      Croce, Carlo M and Capasso, Melania and Gribben, John G},
      title        = {{M}echanisms of {PD}-{L}1/{PD}-1-mediated {CD}8 {T}-cell
                      dysfunction in the context of aging-related immune defects
                      in the {E}µ-{TCL}1 {CLL} mouse model.},
      journal      = {Blood},
      volume       = {126},
      number       = {2},
      issn         = {0006-4971},
      address      = {Washington, DC},
      publisher    = {American Society of Hematology},
      reportid     = {DZNE-2023-00629},
      pages        = {212 - 221},
      year         = {2015},
      abstract     = {T-cell defects, immune suppression, and poor antitumor
                      immune responses are hallmarks of chronic lymphocytic
                      leukemia (CLL), and PD-1/PD-L1 inhibitory signaling has
                      emerged as a major immunosuppressive mechanism. However, the
                      effect of different microenvironments and the confounding
                      influence of aging are poorly understood. The current study
                      uses the Eμ-TCL1 mouse model, which replicates human T-cell
                      defects, as a preclinical platform to longitudinally examine
                      patterns of T-cell dysfunction alongside developing CLL and
                      in different microenvironments, with a focus on PD-1/PD-L1
                      interactions. The development of CLL was significantly
                      associated with changes in T-cell phenotype across all
                      organs and function. Although partly mirrored in aging
                      wild-type mice, CLL-specific T-cell changes were identified.
                      Murine CLL cells highly expressed PD-L1 and PD-L2 in all
                      organs, with high PD-L1 expression in the spleen.
                      CD3(+)CD8(+) T cells from leukemic and aging healthy mice
                      highly expressed PD-1, identifying aging as a confounder,
                      but adoptive transfer experiments demonstrated CLL-specific
                      PD-1 induction. Direct comparisons of PD-1 expression and
                      function between aging CLL mice and controls identified
                      PD-1(+) T cells in CLL as a heterogeneous population with
                      variable effector function. This is highly relevant for
                      therapeutic targeting of CD8(+) T cells, showing the
                      potential of reprogramming and selective subset expansion to
                      restore antitumor immunity.},
      keywords     = {Aging: genetics / Aging: immunology / Animals / B7-H1
                      Antigen: physiology / CD8-Positive T-Lymphocytes: immunology
                      / Cell Differentiation: genetics / Cell Differentiation:
                      immunology / Cells, Cultured / Disease Models, Animal /
                      Immunoglobulin mu-Chains: genetics / Leukemia, Lymphocytic,
                      Chronic, B-Cell: genetics / Leukemia, Lymphocytic, Chronic,
                      B-Cell: immunology / Leukemia, Lymphocytic, Chronic, B-Cell:
                      pathology / Mice / Mice, Transgenic / Programmed Cell Death
                      1 Receptor: physiology / Proto-Oncogene Proteins: genetics /
                      Signal Transduction: immunology / B7-H1 Antigen (NLM
                      Chemicals) / Cd274 protein, mouse (NLM Chemicals) /
                      Immunoglobulin mu-Chains (NLM Chemicals) / Pdcd1 protein,
                      mouse (NLM Chemicals) / Programmed Cell Death 1 Receptor
                      (NLM Chemicals) / Proto-Oncogene Proteins (NLM Chemicals) /
                      Tcl1 protein, mouse (NLM Chemicals)},
      ddc          = {610},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25979947},
      pmc          = {pmc:PMC4497962},
      doi          = {10.1182/blood-2015-02-626754},
      url          = {https://pub.dzne.de/record/258656},
}