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@ARTICLE{Lanz:119439,
      author       = {T. Lanz$^*$ and S. K. Williams and A. Stojic and S.
                      Iwantscheff and J. Sonner$^*$ and C. Grabitz and S.
                      Becker$^*$ and L.-I. Böhler$^*$ and S. R. Mohapatra$^*$ and
                      F. Sahm$^*$ and G. Küblbeck$^*$ and T. Nakamura and H.
                      Funakoshi and C. Opitz$^*$ and W. Wick$^*$ and R. Diem$^*$
                      and M. Platten$^*$},
      title        = {{T}ryptophan-2,3-{D}ioxygenase ({TDO}) deficiency is
                      associated with subclinical neuroprotection in a mouse model
                      of multiple sclerosis.},
      journal      = {Scientific reports},
      volume       = {7},
      issn         = {2045-2322},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-00181},
      pages        = {41271 -},
      year         = {2017},
      abstract     = {The catabolism of tryptophan to immunosuppressive and
                      neuroactive kynurenines is a key metabolic pathway
                      regulating immune responses and neurotoxicity. The
                      rate-limiting step is controlled by
                      indoleamine-2,3-dioxygenase (IDO) and
                      tryptophan-2,3-dioxygenase (TDO). IDO is expressed in
                      antigen presenting cells during immune reactions, hepatic
                      TDO regulates blood homeostasis of tryptophan and neuronal
                      TDO influences neurogenesis. While the role of IDO has been
                      described in multiple immunological settings, little is
                      known about TDO's effects on the immune system.
                      TDO-deficiency is neuroprotective in C. elegans and
                      Drosophila by increasing tryptophan and specific
                      kynurenines. Here we have determined the role of TDO in
                      autoimmunity and neurodegeneration in experimental
                      autoimmune encephalomyelitis (EAE), a model of multiple
                      sclerosis. We created reporter-TDO mice for in vivo imaging
                      to show that hepatic but not CNS TDO expression is activated
                      during EAE. TDO deficiency did not influence myelin-specific
                      T cells, leukocyte infiltration into the CNS, demyelination
                      and disease activity. TDO-deficiency protected from neuronal
                      loss in the spinal cord but not in the optic nerves. While
                      this protection did not translate to an improved overt
                      clinical outcome, our data suggest that spatially distinct
                      neuroprotection is conserved in mammals and support TDO as a
                      potential target for treatment of diseases associated with
                      neurodegeneration.},
      cin          = {G160 / L101 / G161 / G380 / D110 / G370},
      ddc          = {000},
      cid          = {I:(DE-He78)G160-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)G161-20160331 / I:(DE-He78)G380-20160331 /
                      I:(DE-He78)D110-20160331 / I:(DE-He78)G370-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28117398},
      pmc          = {pmc:PMC5259766},
      doi          = {10.1038/srep41271},
      url          = {https://inrepo02.dkfz.de/record/119439},
}