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@ARTICLE{Meyer:300192,
      author       = {S. P. Meyer and R. Bauer and B. Brüne and T. Schmid$^*$},
      title        = {{T}he role of type {I} interferon signaling in myeloid
                      anti-tumor immunity.},
      journal      = {Frontiers in immunology},
      volume       = {16},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DKFZ-2025-00669},
      pages        = {1547466},
      year         = {2025},
      abstract     = {Tumors often arise in chronically inflamed, and thus
                      immunologically highly active niches. While immune cells are
                      able to recognize and remove transformed cells, tumors
                      eventually escape the control of the immune system by
                      shaping their immediate microenvironment. In this context,
                      macrophages are of major importance, as they initially exert
                      anti-tumor functions before they adopt a tumor-associated
                      phenotype that instead inhibits anti-tumor immune responses
                      and even allows for sustaining a smoldering inflammatory,
                      growth promoting tumor microenvironment (TME). Type I
                      interferons (IFNs) are well established modulators of
                      inflammatory reactions. While they have been shown to
                      directly inhibit tumor growth, there is accumulating
                      evidence that they also play an important role in altering
                      immune cell functions within the TME. In the present review,
                      we focus on the impact of type I IFNs on anti-tumor
                      responses, driven by monocytes and macrophages.
                      Specifically, we will provide an overview of tumor-intrinsic
                      factors, which impinge on IFN-stimulated gene (ISG)
                      expression, like the presence of nucleic acids, metabolites,
                      or hypoxia. We will further summarize the current
                      understanding of the consequences of altered IFN responses
                      on macrophage phenotypes, i.e., differentiation,
                      polarization, and functions. For the latter, we will focus
                      on macrophage-mediated tumor cell killing and phagocytosis,
                      as well as on how macrophages affect their environment by
                      secreting cytokines and directly interacting with immune
                      cells. Finally, we will discuss how type I IFN responses in
                      macrophages might affect and should be considered for
                      current and future tumor therapies.},
      subtyp        = {Review Article},
      keywords     = {Humans / Interferon Type I: metabolism / Interferon Type I:
                      immunology / Neoplasms: immunology / Neoplasms: metabolism /
                      Tumor Microenvironment: immunology / Signal Transduction /
                      Animals / Macrophages: immunology / Macrophages: metabolism
                      / Myeloid Cells: immunology / Myeloid Cells: metabolism /
                      hypoxia (Other) / macrophage (Other) / phagocytosis (Other)
                      / polarization (Other) / tumor microenvironment (Other) /
                      type I interferon (Other) / Interferon Type I (NLM
                      Chemicals)},
      cin          = {FM01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40098954},
      pmc          = {pmc:PMC11911529},
      doi          = {10.3389/fimmu.2025.1547466},
      url          = {https://inrepo02.dkfz.de/record/300192},
}