Keratinocytes in atopic dermatitis: inflammatory signals

Area of Science:

• Dermatology
• Immunology
• Cell Biology

Background:

• Atopic dermatitis (AD) is a chronic inflammatory skin condition often preceding allergic airway diseases.
• The pathogenesis of AD is traditionally viewed as allergen-driven, involving antigen-presenting cells and Th2 cells.
• Keratinocytes, as the primary epithelial cells, are increasingly recognized for their role in AD development due to their environmental exposure.

Purpose of the Study:

• To review the multifaceted biological attributes of keratinocytes relevant to atopic dermatitis.
• To highlight the active contribution of keratinocytes to the inflammatory processes in AD.
• To underscore the epithelial cell's role beyond a passive barrier in AD pathogenesis.

Main Methods:

• This is a review article, synthesizing existing research on keratinocytes in AD.
• Key aspects discussed include barrier function, inflammatory mediator production, apoptosis, response to staphylococcal toxins, and immune receptor expression.
• The review focuses on the functional properties of keratinocytes relevant to immune responses.

Main Results:

• Keratinocytes exhibit intrinsic defects in barrier function, contributing to AD.
• They produce inflammatory mediators that exacerbate or sustain allergic inflammation.
• Keratinocyte apoptosis, susceptibility to staphylococcal toxins, and expression of cosignaling and innate immune receptors (e.g., Toll receptors) are significant factors.

Conclusions:

• Keratinocytes play a more active and significant role in the pathogenesis of atopic dermatitis than previously understood.
• Understanding keratinocyte biology is crucial for developing novel therapeutic strategies for AD.
• The epithelium is a key player in initiating and perpetuating AD, not merely a passive bystander.