Proteinase activation: A mechanism for cellular dyshension in pemphigus

K. H. Singer, N. J. Sawka, H. R. Samowitz, G. S. Lazarus

Research output: Contribution to journalArticlepeer-review

Abstract

An in vitro model system using cultured newborn epidermal cells was employed to investigate the binding of pemphigus autoantibody and subsequent loss of adhesion between epidermal cells. Pemphigus antibodies bound to both mouse and human cultured epidermal cells. Incubation of cultured newborn mouse epidermal cells with pemphigus antibody followed by gentle agitation induced loss of adhesion between the epidermal cells and the plastic culture dish. Release of viable epidermal cells from the dish was inhibited by the proteinase inhibitors, soybean trypsin inhibitor and α2-macroglobulin. These observations suggest that pemphigus antibody induces viable epidermal cells to activate cellular proteinases which then degrade the glycocalyx and cause cellular dyshesion and acantholysis.

Original languageEnglish (US)
Pages (from-to)363-367
Number of pages5
JournalJournal of Investigative Dermatology
Volume74
Issue number5
DOIs
StatePublished - 1980

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology

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