Targeting of desmoglein 1 in exfoliative toxin-mediated disease

Cory L. Simpson, Kathleen J. Green, Spiro Getsios

Research output: Contribution to journalReview articlepeer-review


Exfoliative toxin (ET) is secreted by Staphylococcus aureus and has long been known to cause localized or widespread epidermal blistering in humans termed bullous impetigo or staphylococcal scalded-skin syndrome, respectively. While initial hypotheses suggested that ET was a superantigen, sequence and crystallographic analysis characterized the toxin as a serine protease. More recent work determined that ET cleaves a desmosomal cadherin, desmoglein (Dsg)1. This discovery explained the mechanism of toxin-induced blistering, since Dsg1 proteolysis compromises desmosomes, which link keratinocytes and support epidermal integrity. Here, we review clinical findings in ET-mediated disease, the characterization of ET, the molecular pathogenesis of bullous impetigo/staphylococcal scalded-skin syndrome, the structure and function of Dsg1, and current and potential treatments of ET-mediated disease.

Original languageEnglish (US)
Pages (from-to)659-670
Number of pages12
JournalExpert Review of Dermatology
Issue number6
StatePublished - Dec 2010


  • Staphylococcus aureus
  • bullous impetigo
  • desmoglein
  • desmosomal cadherin
  • desmosome
  • exfoliative toxin
  • staphylococcal scalded-skin syndrome

ASJC Scopus subject areas

  • Dermatology


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