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Granulocyte-dependent Autoantibody-induced Skin Blistering

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Published on: October 12, 2012

Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases.

Akiharu Kubo¹, Keisuke Nagao, Masayuki Amagai

¹Department of Dermatology, Keio University School of Medicine, Shinanomachi 35, Shinjuku, Tokyo 160-8582, Japan.

The Journal of Clinical Investigation

|February 2, 2012

Summary

Atopic dermatitis, asthma, and allergies are linked to epidermal barrier dysfunction. Filaggrin gene mutations highlight the skin barrier

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Area of Science:

Dermatology and immunology
Genetics and molecular biology

Background:

Atopic dermatitis often co-occurs with asthma, allergic rhinitis, and food allergies, collectively known as atopic diseases.
Epidermal barrier dysfunction is increasingly recognized as a key factor in the development of atopic diseases.

Purpose of the Study:

To explore the role of epidermal barrier dysfunction in atopic diseases.
To investigate the molecular mechanisms underlying skin barrier function and dysfunction.

Main Methods:

Review of recent discoveries regarding filaggrin gene mutations.
Analysis of the three key components of skin barrier function: stratum corneum, tight junctions, and Langerhans cell network.

Main Results:

Filaggrin gene mutations are identified as predisposing factors for atopic diseases.
The skin barrier comprises air-liquid, liquid-liquid, and immunological components.

Conclusions:

Understanding epidermal barrier function is crucial for elucidating atopic disease pathophysiology.
Further research into molecular events of barrier function can improve understanding of atopic diseases.