Desmoglein as a target in autoimmunity and infection

Research output: Contribution to journalArticle

92 Citations (Scopus)

Abstract

Clinical phenotypes of most diseases are complex. However, once the mechanism behind the scene is clarified, the nature shows amazing beauty. There is a simple logic behind a complex disease. The exact molecular mechanism of the blister formation in staphylococcal scalded skin syndrome (SSSS) remained to be elucidated for 3 decades since exfoliative toxin was discovered by Melish and Glasgow in 1970. A knowledge accumulated to understand the pathogenesis of pemphigus and cell-cell adhesion of keratinocytes led us to solve this question. Desmoglein 1, which is a cadherin type cell-cell adhesion molecule in desmosomes, is targeted in two different skin diseases, pemphigus foliaceus, and SSSS. In pemphigus foliaceus IgG autoantibodies are developed against desmoglein 1 and inhibit its adhesive function with resultant blister formation in the superficial epidermis. In SSSS, exfoliative toxin produced by Staphylococcus aureus specifically binds and cleaves desmoglein 1 with resultant blister formation at the identical site.

Original languageEnglish
Pages (from-to)244-252
Number of pages9
JournalJournal of the American Academy of Dermatology
Volume48
Issue number2 SUPPL.
DOIs
Publication statusPublished - 2003 Feb 1

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Staphylococcal Scalded Skin Syndrome
Desmogleins
Desmoglein 1
Pemphigus
Blister
Exfoliatins
Autoimmunity
Infection
Beauty
Desmosomes
Cell Adhesion Molecules
Cadherins
Keratinocytes
Skin Diseases
Epidermis
Cell Adhesion
Adhesives
Autoantibodies
Staphylococcus aureus
Immunoglobulin G

ASJC Scopus subject areas

  • Dermatology

Cite this

Desmoglein as a target in autoimmunity and infection. / Amagai, Masayuki.

In: Journal of the American Academy of Dermatology, Vol. 48, No. 2 SUPPL., 01.02.2003, p. 244-252.

Research output: Contribution to journalArticle

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