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@ARTICLE{Ghasemi:285587,
      author       = {A. Ghasemi and A. Martinez-Usatorre and L. Li and M. Hicham
                      and A. Guichard and R. Marcone and N. Fournier and B.
                      Torchia and D. Martinez Bedoya and S. Davanture and M.
                      Fernández-Vaquero and C. Fan$^*$ and J. Janzen$^*$ and Y.
                      Mohammadzadeh and R. Genolet and N. Mansouri and M. Wenes
                      and D. Migliorini and M. Heikenwälder$^*$ and M. De Palma},
      title        = {{C}ytokine-armed dendritic cell progenitors for
                      antigen-agnostic cancer immunotherapy.},
      journal      = {Nature cancer},
      volume       = {5},
      number       = {2},
      issn         = {2662-1347},
      address      = {London},
      publisher    = {Nature Research},
      reportid     = {DKFZ-2023-02449},
      pages        = {240-261},
      year         = {2024},
      note         = {2024 Feb;5(2):240-261},
      abstract     = {Dendritic cells (DCs) are antigen-presenting myeloid cells
                      that regulate T cell activation, trafficking and function.
                      Monocyte-derived DCs pulsed with tumor antigens have been
                      tested extensively for therapeutic vaccination in cancer,
                      with mixed clinical results. Here, we present a cell-therapy
                      platform based on mouse or human DC progenitors (DCPs)
                      engineered to produce two immunostimulatory cytokines, IL-12
                      and FLT3L. Cytokine-armed DCPs differentiated into
                      conventional type-I DCs (cDC1) and suppressed tumor growth,
                      including melanoma and autochthonous liver models, without
                      the need for antigen loading or myeloablative host
                      conditioning. Tumor response involved synergy between IL-12
                      and FLT3L and was associated with natural killer and T cell
                      infiltration and activation, M1-like macrophage programming
                      and ischemic tumor necrosis. Antitumor immunity was
                      dependent on endogenous cDC1 expansion and interferon-γ
                      signaling but did not require CD8+ T cell cytotoxicity.
                      Cytokine-armed DCPs synergized effectively with anti-GD2
                      chimeric-antigen receptor (CAR) T cells in eradicating
                      intracranial gliomas in mice, illustrating their potential
                      in combination therapies.},
      cin          = {F180},
      ddc          = {610},
      cid          = {I:(DE-He78)F180-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37996514},
      doi          = {10.1038/s43018-023-00668-y},
      url          = {https://inrepo02.dkfz.de/record/285587},
}