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@ARTICLE{Hanna:178063,
      author       = {B. S. Hanna$^*$ and L. Llaó-Cid$^*$ and M. Iskar$^*$ and
                      P. M. Roessner$^*$ and L. C. Klett$^*$ and J. K. L. Wong$^*$
                      and Y. Paul$^*$ and N. Ioannou and S. Öztürk$^*$ and N.
                      Mack$^*$ and V. Kalter$^*$ and D. Colomer and E. Campo and
                      J. Bloehdorn and S. Stilgenbauer and S. Dietrich$^*$ and M.
                      Schmidt and R. Gabriel and K. Rippe$^*$ and M. Feuerer and
                      A. G. Ramsay and P. Lichter$^*$ and M. Zapatka$^*$ and M.
                      Seiffert$^*$},
      title        = {{I}nterleukin-10 receptor signaling promotes the
                      maintenance of a {PD}-1int {TCF}-1+ {CD}8+ {T} cell
                      population that sustains anti-tumor immunity.},
      journal      = {Immunity},
      volume       = {54},
      number       = {12},
      issn         = {1074-7613},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2021-03072},
      pages        = {2825-2841.e10},
      year         = {2021},
      note         = {#EA:B060#LA:B060# / 2021 Dec 14;54(12):2825-2841.e10},
      abstract     = {T cell exhaustion limits anti-tumor immunity and responses
                      to immunotherapy. Here, we explored the microenvironmental
                      signals regulating T cell exhaustion using a model of
                      chronic lymphocytic leukemia (CLL). Single-cell analyses
                      identified a subset of PD-1hi, functionally impaired CD8+
                      T cells that accumulated in secondary lymphoid organs
                      during disease progression and a functionally competent
                      PD-1int subset. Frequencies of PD-1int TCF-1+ CD8+ T cells
                      decreased upon Il10rb or Stat3 deletion, leading to
                      accumulation of PD-1hi cells and accelerated tumor
                      progression. Mechanistically, inhibition of IL-10R signaling
                      altered chromatin accessibility and disrupted cooperativity
                      between the transcription factors NFAT and AP-1, promoting a
                      distinct NFAT-associated program. Low IL10 expression or
                      loss of IL-10R-STAT3 signaling correlated with increased
                      frequencies of exhausted CD8+ T cells and poor survival in
                      CLL and in breast cancer patients. Thus, balance between
                      PD-1hi, exhausted CD8+ T cells and functional PD-1int
                      TCF-1+ CD8+ T cells is regulated by cell-intrinsic IL-10R
                      signaling, with implications for immunotherapy.},
      keywords     = {CD8(+) T cells (Other) / CLL (Other) / IL-10 (Other) /
                      IL-10R (Other) / NFAT (Other) / PD-1 heterogeneity (Other) /
                      STAT3 (Other) / T cell exhaustion (Other) / TCF-1 (Other) /
                      tumor microenvironment (Other)},
      cin          = {B060 / B066 / D100},
      ddc          = {610},
      cid          = {I:(DE-He78)B060-20160331 / I:(DE-He78)B066-20160331 /
                      I:(DE-He78)D100-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34879221},
      doi          = {10.1016/j.immuni.2021.11.004},
      url          = {https://inrepo02.dkfz.de/record/178063},
}