Impaired Epidermal to Dendritic T Cell Signaling Slows Wound Repair in Aged Skin

Brice E. Keyes, Siqi Liu, Amma Asare, Shruti Naik, John Levorse, Lisa Polak, Catherine P. Lu, Maria Nikolova, Hilda Amalia Pasolli, Elaine Fuchs

Research output: Contribution to journalArticlepeer-review

167 Scopus citations

Abstract

Aged skin heals wounds poorly, increasing susceptibility to infections. Restoring homeostasis after wounding requires the coordinated actions of epidermal and immune cells. Here we find that both intrinsic defects and communication with immune cells are impaired in aged keratinocytes, diminishing their efficiency in restoring the skin barrier after wounding. At the wound-edge, aged keratinocytes display reduced proliferation and migration. They also exhibit a dampened ability to transcriptionally activate epithelial-immune crosstalk regulators, including a failure to properly activate/maintain dendritic epithelial T cells (DETCs), which promote re-epithelialization following injury. Probing mechanism, we find that aged keratinocytes near the wound edge don't efficiently upregulate Skints or activate STAT3. Notably, when epidermal Stat3, Skints, or DETCs are silenced in young skin, re-epithelialization following wounding is perturbed. These findings underscore epithelial-immune crosstalk perturbations in general, and Skints in particular, as critical mediators in the age-related decline in wound-repair.

Original languageEnglish (US)
Pages (from-to)1323-1338.e14
JournalCell
Volume167
Issue number5
DOIs
StatePublished - Nov 17 2016
Externally publishedYes

Keywords

  • Aging
  • DETC
  • STAT3
  • Skint
  • epidermal-immune cell cross-talk
  • re-epithelialization
  • wound healing

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology

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