Human keratinocytes' response to injury upregulates CCL20 and other genes linking innate and adaptive immunity Academic Article uri icon


MeSH Major

  • Chemokine CCL20
  • Epidermis
  • Immunity, Innate
  • Keratinocytes
  • Psoriasis


  • In the early stages of wound healing, keratinocytes (KCs) become "activated" and release inflammatory molecules such as IL-1 and IL-8, which are linked to innate immune responses and neutrophil recruitment. It is unclear, however, whether KCs release molecules linked to adaptive immune responses, e.g., CCL20, in their early state of activation without signals from infiltrating T cells. This study aims to isolate the immediate alterations in protective and inflammatory gene expression that occur in epidermal KCs, with a particular focus on molecules associated with cell-mediated immunity. We used dispase-separated epidermis, followed by intercellular disassociation by trypsinization, as a model for epidermal injury. We obtained a pure population of KCs using flow cytometry. As a control for uninjured epidermis, we performed laser capture microdissection on normal human skin. Sorted KCs had an early burst of upregulated gene expression, which included CCL20, IL-15, IL-23A, IFN-κ, and several antimicrobial peptides. Our results provide insight into the potential role of KCs as contributors to cell-mediated inflammation, and expand knowledge about gene modulation that occurs during early wound healing. Our findings may be relevant to cutaneous diseases such as psoriasis, where micro-injury can trigger the formation of psoriatic plaques at the site of trauma.

publication date

  • January 2012



  • Academic Article



  • eng

PubMed Central ID

  • PMC3235229

Digital Object Identifier (DOI)

  • 10.1038/jid.2011.262

PubMed ID

  • 21881590

Additional Document Info

start page

  • 105

end page

  • 13


  • 132


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