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Defective cell-cell adhesion in the epidermis

J R Stanley1

  • 1Dermatology Branch, National Cancer Institute, Bethesda, MD 20892, USA.

Ciba Foundation Symposium
|January 1, 1995
PubMed
Summary
This summary is machine-generated.

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Autoantibodies targeting desmoglein 1 and desmoglein 3 cause blistering skin diseases by disrupting epidermal cell adhesion. Further research is needed to understand the exact cell biological function of desmogleins.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Immunology

Background:

  • Pemphigus foliaceus and pemphigus vulgaris are severe blistering skin diseases.
  • Loss of epidermal cell adhesion, induced by autoantibodies, underlies these conditions.

Purpose of the Study:

  • To identify and characterize the antigens targeted by autoantibodies in pemphigus.
  • To investigate the role of desmogleins in epidermal cell adhesion.

Main Methods:

  • Molecular cloning was used to identify pemphigus antigens.
  • Analysis of desmoglein structure and homology to cadherins.

Main Results:

  • Pemphigus foliaceus antigen is desmoglein 1 (dsg-1); Pemphigus vulgaris antigen is desmoglein 3 (dsg-3).

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  • Both desmogleins are members of the cadherin superfamily and link to plakoglobin.
  • Antibodies against dsg-3 disrupt epidermal cell adhesion, suggesting a role in adhesion, though direct evidence is lacking.

    • Conclusions:

    • Desmogleins are implicated in epidermal cell adhesion.
    • The precise cell biological function of desmogleins requires further investigation.