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@ARTICLE{Sektioglu:130541,
      author       = {I. M. Sektioglu$^*$ and R. Carretero$^*$ and N. Bender$^*$
                      and C. Bogdan and N. Garbi and V. Umansky$^*$ and L.
                      Umansky$^*$ and K. Urban$^*$ and C. Knebel Döberitz$^*$ and
                      V. Somasundaram and D. Wink and P. Beckhove$^*$ and G.
                      Hämmerling$^*$},
      title        = {{M}acrophage-derived nitric oxide initiates {T}-cell
                      diapedesis and tumor rejection.},
      journal      = {OncoImmunology},
      volume       = {5},
      number       = {10},
      issn         = {2162-402X},
      address      = {Austin, Tex.},
      publisher    = {Landes Bioscience},
      reportid     = {DKFZ-2017-05620},
      pages        = {e1204506 -},
      year         = {2016},
      abstract     = {In tumor biology, nitric oxide (NO) is generally regarded
                      as an immunosuppressive molecule that impedes T-cell
                      functions and activation of endothelial cells. Contrasting
                      with this view, we here describe a critical role for NO
                      derived from inducible nitric oxide (iNOS)-expressing tumor
                      macrophages in T-cell infiltration and tumor rejection as
                      shown by iNOS gene deletion, inhibition of iNOS, or NO
                      donors. Specifically, macrophage-derived NO was found to
                      induce on tumor vessels adhesion molecules that were
                      required for T-cell extravasation. Experiments with human
                      endothelial cells revealed a bimodal dose-dependent effect
                      of NO. High doses of NO donors were indeed suppressive but
                      lower, more physiological concentrations, induced adhesion
                      molecules in an NFkB-dependent pathway and preferentially
                      activated transcription of genes involved in lymphocyte
                      diapedesis. iNOS(+) macrophages in tumors appear to generate
                      precisely the amount of NO that promotes endothelial
                      activation and T-cell infiltration. These results will be
                      valuable for the development of strategies designed to
                      overcome the paucity of T-cell infiltration into tumors that
                      is a major obstacle in clinical cancer immunotherapy.},
      cin          = {D030 / G181 / G300 / G808 / D015},
      ddc          = {610},
      cid          = {I:(DE-He78)D030-20160331 / I:(DE-He78)G181-20160331 /
                      I:(DE-He78)G300-20160331 / I:(DE-He78)G808-20160331 /
                      I:(DE-He78)D015-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27853636},
      pmc          = {pmc:PMC5087300},
      doi          = {10.1080/2162402X.2016.1204506},
      url          = {https://inrepo02.dkfz.de/record/130541},
}