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@ARTICLE{Popovic:120542,
      author       = {Z. Popovic$^*$ and M. Embgenbroich and F. Chessa$^*$ and V.
                      Nordström$^*$ and M. Bonrouhi$^*$ and T. Hielscher$^*$ and
                      N. Gretz and S. Wang$^*$ and D. Mathow$^*$ and T. Quast and
                      J.-G. Schloetel and W. Kolanus and S. Burgdorf and H.-J.
                      Gröne$^*$},
      title        = {{H}yperosmolarity impedes the cross-priming competence of
                      dendritic cells in a {TRIF}-dependent manner.},
      journal      = {Scientific reports},
      volume       = {7},
      number       = {1},
      issn         = {2045-2322},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-00971},
      pages        = {311},
      year         = {2017},
      abstract     = {Tissue osmolarity varies among different organs and can be
                      considerably increased under pathologic conditions.
                      Hyperosmolarity has been associated with altered stimulatory
                      properties of immune cells, especially macrophages and
                      dendritic cells. We have recently reported that dendritic
                      cells upon exposure to hypertonic stimuli shift their
                      profile towards a macrophage-M2-like phenotype, resulting in
                      attenuated local alloreactivity during acute kidney graft
                      rejection. Here, we examined how hyperosmotic
                      microenvironment affects the cross-priming capacity of
                      dendritic cells. Using ovalbumin as model antigen, we showed
                      that exposure of dendritic cells to hyperosmolarity strongly
                      inhibits activation of antigen-specific T cells despite
                      enhancement of antigen uptake, processing and presentation.
                      We identified TRIF as key mediator of this phenomenon.
                      Moreover, we detected a hyperosmolarity-triggered,
                      TRIF-dependent clustering of MHCI loaded with the
                      ovalbumin-derived epitope, but not of overall MHCI
                      molecules, providing a possible explanation for a reduced T
                      cell activation. Our findings identify dendritic cells as
                      important players in hyperosmolarity-mediated immune
                      imbalance and provide evidence for a novel pathway of
                      inhibition of antigen specific CD8(+) T cell response in a
                      hypertonic micromilieu.},
      cin          = {G130 / C060},
      ddc          = {000},
      cid          = {I:(DE-He78)G130-20160331 / I:(DE-He78)C060-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28331179},
      pmc          = {pmc:PMC5428499},
      doi          = {10.1038/s41598-017-00434-y},
      url          = {https://inrepo02.dkfz.de/record/120542},
}