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@ARTICLE{Stachura:278581,
      author       = {P. Stachura and W. Liu and H. C. Xu and A. Wlodarczyk and
                      O. Stencel and P. Pandey and M. Vogt and S. Bhatia and D.
                      Picard$^*$ and M. Remke$^*$ and K. S. Lang and D.
                      Häussinger and B. Homey and P. A. Lang and A. Borkhardt and
                      A. A. Pandyra},
      title        = {{U}nleashing {T} cell anti-tumor immunity: new potential
                      for 5-{N}onloxytryptamine as an agent mediating {MHC}-{I}
                      upregulation in tumors.},
      journal      = {Molecular cancer},
      volume       = {22},
      number       = {1},
      issn         = {1476-4598},
      address      = {London},
      publisher    = {Biomed Central},
      reportid     = {DKFZ-2023-01662},
      pages        = {136},
      year         = {2023},
      abstract     = {New therapies are urgently needed in melanoma, particularly
                      in late-stage patients not responsive to immunotherapies and
                      kinase inhibitors. To uncover novel potentiators of T cell
                      anti-tumor immunity, we carried out an ex vivo
                      pharmacological screen and identified 5-Nonyloxytryptamine
                      (5-NL), a serotonin agonist, as increasing the ability of T
                      cells to target tumor cells.The pharmacological screen
                      utilized lymphocytic choriomeningitis virus (LCMV)-primed
                      splenic T cells and melanoma B16.F10 cells expressing the
                      LCMV gp33 CTL epitope. In vivo tumor growth in C57BL/6 J and
                      NSG mice, in vivo antibody depletion, flow cytometry,
                      immunoblot, CRISPR/Cas9 knockout, histological and RNA-Seq
                      analyses were used to decipher 5-NL's immunomodulatory
                      effects in vitro and in vivo.5-NL delayed tumor growth in
                      vivo and the phenotype was dependent on the hosts' immune
                      system, specifically CD8+ T cells. 5-NL's pro-immune effects
                      were not directly consequential to T cells. Rather, 5-NL
                      upregulated antigen presenting machinery in melanoma and
                      other tumor cells in vitro and in vivo without increasing
                      PD-L1 expression. Mechanistic studies indicated that 5-NL's
                      induced MHC-I expression was inhibited by pharmacologically
                      preventing cAMP Response Element-Binding Protein (CREB)
                      phosphorylation. Importantly, 5-NL combined with anti-PD1
                      therapy showed significant improvement when compared to
                      single anti-PD-1 treatment.This study demonstrates novel
                      therapeutic opportunities for augmenting immune responses in
                      poorly immunogenic tumors.},
      keywords     = {5-Nonyloxytryptamine (5-NL) (Other) / Antigen-presenting
                      machinery (Other) / CD8+ T cells (Other) / Cold tumors
                      (Other) / Immunotherapy (Other) / cAMP response
                      element-binding protein (CREB) (Other)},
      cin          = {ED01},
      ddc          = {570},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37582744},
      doi          = {10.1186/s12943-023-01833-8},
      url          = {https://inrepo02.dkfz.de/record/278581},
}