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@ARTICLE{Fischer:301578,
      author       = {B. Fischer and A. Kolb and E. Focaccia and T. Kübelbeck
                      and M. Klein and D. Löck and F. Bork and F. Engelmann and
                      M. Casari and E. Mazza and C. Deppermann and A. N. R.
                      Weber$^*$ and M. Wittmann and B. Schittek and K.
                      Schulze-Osthoff$^*$ and D. Kramer},
      title        = {{NOD}2-induced {I}κ{B}ζ mediates a protective host
                      response against epicutaneous {S}taphylococcus aureus
                      infection.},
      journal      = {The journal of investigative dermatology},
      volume       = {nn},
      issn         = {0022-202X},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2025-01086},
      pages        = {nn},
      year         = {2025},
      note         = {epub},
      abstract     = {IκBζ, an atypical and largely unknown member of the IκB
                      family, is a transcriptional coactivator of selective immune
                      functions. Here, we investigated the role of
                      keratinocyte-derived IκBζ upon infection with a
                      multidrug-resistant S. aureus strain. Infection of
                      keratinocytes rapidly induced IκBζ expression, leading to
                      an elevated expression of antimicrobial peptides,
                      IL-17/IL-36-responsive genes, and proteins involved in skin
                      barrier function. Conversely, loss of IκBζ resulted in
                      increased S. aureus internalization, epidermal tissue
                      damage, and severe skin infections in vivo. This impaired
                      host defense upon IκBζ depletion was characterized by
                      reduced antimicrobial peptide expression, and diminished
                      recruitment of neutrophils and CD4+ T-cells. Importantly, S.
                      aureus-induced IκBζ expression required the
                      internalization of the bacteria and its sensing by the
                      intracellular receptor NOD2, which triggered IκBζ and its
                      target gene expression. Thus, we identified NOD2-IκBζ
                      signaling as a novel pathway acting as a key mediator for a
                      protective host defense against pathogenic S. aureus
                      infections in the skin.},
      keywords     = {IκBζ (Other) / NFKBIZ (Other) / NOD2 (Other) /
                      Staphylococcus aureus (Other) / TLR2 (Other) / keratinocytes
                      (Other)},
      cin          = {TU01},
      ddc          = {610},
      cid          = {I:(DE-He78)TU01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40412468},
      doi          = {10.1016/j.jid.2025.04.036},
      url          = {https://inrepo02.dkfz.de/record/301578},
}