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Differences in the expression of pemphigus antigens during epidermal differentiation
K Iwatsuki1, H Harada, R Yokote
1Department of Dermatology, Fukushima Medical College, Japan.
The British Journal of Dermatology
|August 1, 1995
Summary
The study reveals that a decrease in desmoglein 3 (Dsg3) during epidermal differentiation may cause pemphigus vulgaris (PV). This contrasts with pemphigus foliaceus (PF), where desmoglein 1 (Dsg1) becomes dominant.
Area of Science:
- Dermatology
- Cell Biology
- Immunology
Background:
- Pemphigus vulgaris (PV) and pemphigus foliaceus (PF) are autoimmune blistering diseases.
- Autoantibodies target specific desmogleins: Dsg3 in PV and Dsg1 in PF.
- Understanding desmoglein expression during keratinocyte differentiation is crucial for elucidating disease mechanisms.
Purpose of the Study:
- To investigate the expression patterns of desmoglein 1 (Dsg1) and desmoglein 3 (Dsg3) during keratinocyte stratification.
- To correlate desmoglein expression changes with the histogenesis of PV and PF.
Main Methods:
- Culture of normal human keratinocytes.
- Immunoblotting to determine desmoglein protein levels.
- Analysis of desmoglein mRNA expression.
- Immunohistochemical staining with patient sera.
Main Results:
- Both Dsg1 and Dsg3 proteins and mRNA were expressed in cultured keratinocytes.
- Dsg3 expression decreased relative to total desmogleins as keratinocytes stratified.
- Dsg1 became predominant in fully stratified keratinocytes, with reduced PV antigen expression.
Conclusions:
- The relative decrease of Dsg3 during epidermal differentiation may induce suprabasal acantholysis in PV.
- Differential desmoglein expression during stratification plays a role in the distinct clinical presentations of PV and PF.