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@ARTICLE{Gambichler:169037,
      author       = {T. Gambichler and S. Hessam and M. Skrygan and M. Bakirtzi
                      and D. Kasakovski$^*$ and F. G. Bechara},
      title        = {{NOD}2 signalling in hidradenitis suppurativa.},
      journal      = {Clinical and experimental dermatology},
      volume       = {46},
      number       = {8},
      issn         = {1365-2230},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DKFZ-2021-01204},
      pages        = {1488-1494},
      year         = {2021},
      note         = {2021 Dec;46(8):1488-1494},
      abstract     = {Hidradenitis suppurativa (HS) is associated with
                      dysregulated immune responses including altered expression
                      of cytokines, chemokines, and antimicrobial peptides and
                      proteins (AMPs).To evaluate the expression of NOD2 and
                      related factors in HS skin samples and keratinocyte
                      cultures.We performed RT-PCR for NOD2, RIP2, CARL,
                      SKALP/elafin, human ß-defensin 2 (hBD2), LL37, psoriasin,
                      RNAse7 in lesional and non-lesional skin of 19 HS patients
                      and keratinocyte cultures (unstimulated, MDP-stimulated,
                      PAM-stimulated) from and non-lesional skin.We observed
                      significantly elevated mRNA expression for NOD2 (P =
                      0.0039), hBD2 (P = 0.018), RNase7 (P = 0.0003), psoriasin
                      (P = 0.0053), and SKALP/elafin (P = 0.020) in lesional skin
                      when compared to non-lesional skin. We found a significant
                      correlation between NOD2 mRNA and hBD2 (r = 46; P = 0.039),
                      psoriasin (r = 0.67; P = 0.0016), SKALP/elafin (r = 0.65; P
                      = 0.0026). In unstimulated, PAM-stimulated, and
                      MDP-stimulated normal keratinocytes, NOD2, RIP2, CARL, and
                      SKALP/elafin expression significantly (P < 0.05) increased
                      from 6 h to 48 h. In unstimulated, PAM-stimulated, and
                      MDP-stimulated HS keratinocytes, RIP2, CARL, and
                      SKALP/elafin expression significantly (P < 0.05) declined
                      from 6 h to 48 h. mRNA expression of HS keratinocytes at 6 h
                      was significantly increased for NOD2 (unstimulated, PAM,
                      MDP), CARL (unstimulated, PAM, MDP), and SALP/elafin
                      (unstimulated, PAM) as compared to normal keratinocytes.We
                      have shown for the first time that the NOD2 signalling is
                      activated in HS and might contribute to the pathogenesis via
                      induction of AMPs and activation of other pathways such as
                      NFκB signalling.},
      cin          = {A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34056759},
      doi          = {10.1111/ced.14773},
      url          = {https://inrepo02.dkfz.de/record/169037},
}