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@ARTICLE{AbuHejleh:271002,
      author       = {A. Abu Hejleh$^*$ and K. Huck$^*$ and K. Jähne$^*$ and C.
                      Tan$^*$ and T. Lanz and L. Epping and J. Sonner and S. Meuth
                      and A. Henneberg$^*$ and C. Opitz$^*$ and C. Herold-Mende
                      and F. Sahm$^*$ and M. Platten$^*$ and K. Sahm$^*$},
      title        = {{E}ndothelial {I}ndoleamine-2,3-{D}ioxygenase-1 is not
                      {C}ritically {I}nvolved in {R}egulating {A}ntitumor
                      {I}mmunity in the {C}entral {N}ervous {S}ystem},
      journal      = {International journal of tryptophan research},
      volume       = {16},
      issn         = {1178-6469},
      address      = {Thousand Oaks, CA},
      publisher    = {Sage Publications},
      reportid     = {DKFZ-2023-00355},
      pages        = {117864692311531},
      year         = {2023},
      note         = {#EA:D170#LA:D170#},
      abstract     = {The vascular niche of malignant gliomas is a key
                      compartment that shapes the immunosuppressive brain tumor
                      microenvironment (TME). The blood-brain-barrier (BBB)
                      consisting of specialized endothelial cells (ECs) and
                      perivascular cells forms a tight anatomical and functional
                      barrier critically controlling transmigration and effector
                      function of immune cells. During neuroinflammation and tumor
                      progression, the metabolism of the essential amino acid
                      tryptophan (Trp) to metabolites such as kynurenine has long
                      been identified as an important metabolic pathway
                      suppressing immune responses. Previous studies have
                      demonstrated that indoleamine-2,3-dioxygenase-1 (IDO1), a
                      key rate-limiting enzyme in tryptophan catabolism, is
                      expressed within the TME of high-grade gliomas. Here, we
                      investigate the role of endothelial IDO1 (eIDO1) expression
                      for brain tumor immunity. Single-cell RNA sequencing data
                      revealed that in human glioma tissue, IDO1 is predominantly
                      expressed by activated ECs showing a JAK/STAT signaling
                      pathway-related CXCL11+ gene expression signature. In a
                      syngeneic experimental glioma model, eIDO1 is induced by
                      low-dose tumor irradiation. However, cell type-specific
                      ablation of eIDO1 in experimental gliomas did not alter
                      frequency and phenotype of tumor-infiltrating T cells nor
                      tumor growth. Taken together these data argue against a
                      dominant role of eIDO1 for brain tumor immunity.},
      cin          = {D170 / HD01 / B350 / B300},
      ddc          = {540},
      cid          = {I:(DE-He78)D170-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)B350-20160331 / I:(DE-He78)B300-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36798537},
      doi          = {10.1177/11786469231153111},
      url          = {https://inrepo02.dkfz.de/record/271002},
}