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@ARTICLE{Meister:136090,
      author       = {M. Meister$^*$ and M. Papatriantafyllou$^*$ and V.
                      Nordström$^*$ and V. Kumar and J. Ludwig$^*$ and K. O. Lui
                      and A. S. Boyd and Z. Popovic$^*$ and T. H. Fleming and G.
                      Moldenhauer$^*$ and P. P. Nawroth and H.-J. Gröne$^*$ and
                      H. Waldmann$^*$ and T. Oelert$^*$ and B. Arnold$^*$},
      title        = {{D}ickkopf-3, a tissue-derived modulator of local {T}-cell
                      responses.},
      journal      = {Frontiers in immunology},
      volume       = {6},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DKFZ-2018-00785},
      pages        = {78},
      year         = {2015},
      abstract     = {The adaptive immune system protects organisms from harmful
                      environmental insults. In parallel, regulatory mechanisms
                      control immune responses in order to assure preservation of
                      organ integrity. Yet, molecules involved in the control of
                      T-cell responses in peripheral tissues are poorly
                      characterized. Here, we investigated the function of
                      Dickkopf-3 in the modulation of local T-cell reactivity.
                      Dkk3 is a secreted, mainly tissue-derived protein with
                      highest expression in organs considered as immune-privileged
                      such as the eye, embryo, placenta, and brain. While T-cell
                      development and activation status in naïve Dkk3-deficient
                      mice was comparable to littermate controls, we found that
                      Dkk3 contributes to the immunosuppressive microenvironment
                      that protects transplanted, class-I mismatched embryoid
                      bodies from T-cell-mediated rejection. Moreover, genetic
                      deletion or antibody-mediated neutralization of Dkk3 led to
                      an exacerbated experimental autoimmune encephalomyelitis
                      (EAE). This phenotype was accompanied by a change of T-cell
                      polarization displayed by an increase of IFNγ-producing T
                      cells within the central nervous system. In the wild-type
                      situation, Dkk3 expression in the brain was up-regulated
                      during the course of EAE in an IFNγ-dependent manner. In
                      turn, Dkk3 decreased IFNγ activity and served as part of a
                      negative feedback mechanism. Thus, our findings suggest that
                      Dkk3 functions as a tissue-derived modulator of local CD4(+)
                      and CD8(+) T-cell responses.},
      cin          = {G130 / D050},
      ddc          = {610},
      cid          = {I:(DE-He78)G130-20160331 / I:(DE-He78)D050-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25759692},
      pmc          = {pmc:PMC4338807},
      doi          = {10.3389/fimmu.2015.00078},
      url          = {https://inrepo02.dkfz.de/record/136090},
}