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@ARTICLE{Mothes:267547,
      author       = {R. Mothes and A. Pascual-Reguant and R. Koehler and J.
                      Liebeskind and A. Liebheit and S. Bauherr and L. Philipsen
                      and C. Dittmayer and M. Laue and R. von Manitius and S.
                      Elezkurtaj and P. Durek and F. Heinrich and G. A. Heinz and
                      G. M. Guerra and B. Obermayer and J. Meinhardt and J. Ihlow
                      and J. Radke$^*$ and F. L. Heppner and P. Enghard and H.
                      Stockmann and T. Aschman and J. Schneider and V. M. Corman
                      and L. E. Sander and M.-F. Mashreghi and T. Conrad and A. C.
                      Hocke and R. A. Niesner and H. Radbruch and A. E. Hauser},
      title        = {{D}istinct tissue niches direct lung immunopathology via
                      {CCL}18 and {CCL}21 in severe {COVID}-19.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-00325},
      pages        = {791},
      year         = {2023},
      abstract     = {Prolonged lung pathology has been associated with COVID-19,
                      yet the cellular and molecular mechanisms behind this
                      chronic inflammatory disease are poorly understood. In this
                      study, we combine advanced imaging and spatial
                      transcriptomics to shed light on the local immune response
                      in severe COVID-19. We show that activated adventitial
                      niches are crucial microenvironments contributing to the
                      orchestration of prolonged lung immunopathology.
                      Up-regulation of the chemokines CCL21 and CCL18 associates
                      to endothelial-to-mesenchymal transition and tissue fibrosis
                      within these niches. CCL21 over-expression additionally
                      links to the local accumulation of T cells expressing the
                      cognate receptor CCR7. These T cells are imprinted with an
                      exhausted phenotype and form lymphoid aggregates that can
                      organize in ectopic lymphoid structures. Our work proposes
                      immune-stromal interaction mechanisms promoting a
                      self-sustained and non-resolving local immune response that
                      extends beyond active viral infection and perpetuates tissue
                      remodeling.},
      cin          = {BE01},
      ddc          = {500},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36774347},
      doi          = {10.1038/s41467-023-36333-2},
      url          = {https://inrepo02.dkfz.de/record/267547},
}