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@ARTICLE{Ni:157001,
      author       = {J. Ni$^*$ and X. Wang$^*$ and A. Stojanovic$^*$ and Q.
                      Zhang$^*$ and M. Wincher and L. K. Bühler$^*$ and A.
                      Arnold$^*$ and M. P. Correia$^*$ and M. Winkler and P.-S.
                      Koch and V. Sexl and T. Höfer$^*$ and A. Cerwenka$^*$},
      title        = {{S}ingle-{C}ell {RNA} {S}equencing of
                      {T}umor-{I}nfiltrating {NK} {C}ells {R}eveals that
                      {I}nhibition of {T}ranscription {F}actor {HIF}-1α
                      {U}nleashes {NK} {C}ell {A}ctivity.},
      journal      = {Immunity},
      volume       = {52},
      number       = {6},
      issn         = {1074-7613},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2020-01298},
      pages        = {1075 - 1087.e8},
      year         = {2020},
      abstract     = {Enhancing immune cell functions in tumors remains a major
                      challenge in cancer immunotherapy. Hypoxia is a common
                      feature of solid tumors, and cells adapt by upregulating the
                      transcription factor HIF-1α. Here, we defined the
                      transcriptional landscape of mouse tumor-infiltrating
                      natural killer (NK) cells by using single-cell RNA
                      sequencing. Conditional deletion of Hif1a in NK cells
                      resulted in reduced tumor growth, elevated expression of
                      activation markers, effector molecules, and an enriched
                      NF-κB pathway in tumor-infiltrating NK cells.
                      Interleukin-18 (IL-18) from myeloid cells was required for
                      NF-κB activation and the enhanced anti-tumor activity of
                      Hif1a-/- NK cells. Extended culture with an HIF-1α
                      inhibitor increased human NK cell responses. Low HIF1A
                      expression was associated with high expression of IFNG in
                      human tumor-infiltrating NK cells, and an enriched
                      NK-IL18-IFNG signature in solid tumors correlated with
                      increased overall patient survival. Thus, inhibition of
                      HIF-1α unleashes NK cell anti-tumor activity and could be
                      exploited for cancer therapy.},
      cin          = {B086 / D080},
      ddc          = {610},
      cid          = {I:(DE-He78)B086-20160331 / I:(DE-He78)D080-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32445619},
      doi          = {10.1016/j.immuni.2020.05.001},
      url          = {https://inrepo02.dkfz.de/record/157001},
}