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@ARTICLE{Papaioannou:277768,
      author       = {S. Papaioannou and J.-X. See and M. Jeong and C. De La
                      Torre and V. Ast and P.-S. Reiners-Koch and A. Sati$^*$ and
                      C. Mogler and M. Platten$^*$ and A. Cerwenka and A.
                      Stojanovic},
      title        = {{L}iver sinusoidal endothelial cells orchestrate {NK} cell
                      recruitment and activation in acute inflammatory liver
                      injury.},
      journal      = {Cell reports},
      volume       = {42},
      number       = {8},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2023-01483},
      pages        = {112836},
      year         = {2023},
      abstract     = {Liver sinusoidal endothelial cells (LSECs) rapidly clear
                      lipopolysaccharide (LPS) from the bloodstream and establish
                      intimate contact with immune cells. However, their role in
                      regulating liver inflammation remains poorly understood. We
                      show that LSECs modify their chemokine expression profile
                      driven by LPS or interferon-γ (IFN-γ), resulting in the
                      production of the myeloid- or lymphoid-attracting chemokines
                      CCL2 and CXCL10, respectively, which accumulate in the serum
                      of LPS-challenged animals. Natural killer (NK) cell exposure
                      to LSECs in vitro primes NK cells for higher production of
                      IFN-γ in response to interleukin-12 (IL-12) and IL-18. In
                      livers of LPS-injected mice, NK cells are the major
                      producers of this cytokine. In turn, LSECs require exposure
                      to IFN-γ for CXCL10 expression, and endothelial-specific
                      Cxcl10 gene deletion curtails NK cell accumulation in the
                      inflamed livers. Thus, LSECs respond to both LPS and
                      immune-derived signals and fuel a positive feedback loop of
                      immune cell attraction and activation in the inflamed liver
                      tissue.},
      keywords     = {CP: Immunology (Other) / CXCL10 (Other) / IFN-γ (Other) /
                      LPS (Other) / LSECs (Other) / NK cell migration (Other) / NK
                      cells (Other) / liver endothelial cells (Other) / liver
                      inflammation (Other)},
      cin          = {D170 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)D170-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37471222},
      doi          = {10.1016/j.celrep.2023.112836},
      url          = {https://inrepo02.dkfz.de/record/277768},
}