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@ARTICLE{Lanz:124448,
      author       = {T. Lanz$^*$ and S. Becker$^*$ and S. R. Mohapatra$^*$ and
                      C. Opitz$^*$ and W. Wick$^*$ and M. Platten$^*$},
      title        = {{S}uppression of {T}h1 differentiation by tryptophan
                      supplementation in vivo.},
      journal      = {Amino acids},
      volume       = {49},
      number       = {7},
      issn         = {1438-2199},
      address      = {Wien [u.a.]},
      publisher    = {Springer},
      reportid     = {DKFZ-2017-01325},
      pages        = {1169 - 1175},
      year         = {2017},
      abstract     = {Metabolism of the essential amino acid tryptophan (trp) is
                      a key endogenous immunosuppressive pathway restricting
                      inflammatory responses. Tryptophan metabolites promote
                      regulatory T cell (Treg) differentiation and suppress
                      proinflammatory T helper cell (Th)1 and Th17 phenotypes. It
                      has been shown that treatment with natural and synthetic
                      tryptophan metabolites can suppress autoimmune
                      neuroinflammation in preclinical animal models. Here, we
                      tested if oral intake of tryptophan would increase
                      immunosuppressive tryptophan metabolites and ameliorate
                      autoimmune neuroinflammation as a safe approach to treat
                      autoimmune disorders like multiple sclerosis (MS). Without
                      oral supplementation, systemic kynurenine levels decrease
                      during the initiation phase of experimental autoimmune
                      encephalomyelitis (EAE), a mouse model of MS, indicating
                      systemic activation of tryptophan metabolism. Daily oral
                      gavage of up to 10 mg/mouse/day was safe and increased
                      serum kynurenine levels by more than 20-fold for more than
                      3 h after the gavage. While this treatment resulted in
                      suppression of myelin-specific Th1 responses, there was no
                      relevant impact on clinical disease activity. These data
                      show that oral trp supplementation at subtoxic
                      concentrations suppresses antigen-specific Th1 responses,
                      but suggest that the increase in trp metabolites is not
                      sustained enough to impact neuroinflammation.},
      cin          = {G160 / L101 / G161 / G370},
      ddc          = {540},
      cid          = {I:(DE-He78)G160-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)G161-20160331 / 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:28421297},
      doi          = {10.1007/s00726-017-2415-4},
      url          = {https://inrepo02.dkfz.de/record/124448},
}