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@ARTICLE{Meister:127092,
      author       = {M. Meister$^*$ and A. Tounsi$^*$ and E. Gaffal and T. Bald
                      and M. Papatriantafyllou$^*$ and J. Ludwig$^*$ and G.
                      Pougialis$^*$ and F. Bestvater$^*$ and L. Klotz and G.
                      Moldenhauer$^*$ and T. Tüting and G. Hämmerling$^*$ and B.
                      Arnold$^*$ and T. Oelert$^*$},
      title        = {{S}elf-{A}ntigen {P}resentation by {K}eratinocytes in the
                      {I}nflamed {A}dult {S}kin {M}odulates {T}-{C}ell
                      {A}uto-{R}eactivity.},
      journal      = {The journal of investigative dermatology},
      volume       = {135},
      number       = {8},
      issn         = {0022-202X},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2017-03118},
      pages        = {1996 - 2004},
      year         = {2015},
      abstract     = {Keratinocytes have a pivotal role in the regulation of
                      immune responses, but the impact of antigen presentation by
                      these cells is still poorly understood, particularly in a
                      situation where the antigen will be presented only in adult
                      life. Here, we generated a transgenic mouse model in which
                      keratinocytes exclusively present a myelin basic protein
                      (MBP) peptide covalently linked to the major
                      histocompatibility complex class II β-chain, solely under
                      inflammatory conditions. In these mice, inflammation caused
                      by epicutaneous contact sensitizer treatment resulted in
                      keratinocyte-mediated expansion of MBP-specific CD4(+) T
                      cells in the skin. Moreover, repeated contact sensitizer
                      application preceding a systemic MBP immunization reduced
                      the reactivity of the respective CD4(+) T cells and lowered
                      the symptoms of the resulting experimental autoimmune
                      encephalomyelitis. This downregulation was CD4(+)
                      T-cell-mediated and dependent on the presence of the immune
                      modulator Dickkopf-3. Thus, presentation of a neo
                      self-antigen by keratinocytes in the inflamed, adult skin
                      can modulate CD4(+) T-cell auto-aggression at a distal
                      organ.},
      keywords     = {4-ethoxymethylene-2-phenyl-2-oxazoline-5-one (NLM
                      Chemicals) / Autoantigens (NLM Chemicals) / Cyclopropanes
                      (NLM Chemicals) / Dkk3 protein, mouse (NLM Chemicals) /
                      Intercellular Signaling Peptides and Proteins (NLM
                      Chemicals) / Myelin Basic Protein (NLM Chemicals) / Oxazoles
                      (NLM Chemicals) / diphenylcyclopropenone (NLM Chemicals)},
      cin          = {G130 / W210 / D050},
      ddc          = {610},
      cid          = {I:(DE-He78)G130-20160331 / I:(DE-He78)W210-20160331 /
                      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:25835957},
      doi          = {10.1038/jid.2015.130},
      url          = {https://inrepo02.dkfz.de/record/127092},
}