Atopic dermatitis is an allergy affecting approximately 10% of the Japanese population, with symptoms closely related to social stress. In socially active adults, the disease often becomes chronic.

In affected areas, infiltrating immune cells secrete inflammatory cytokines, which contribute to symptom development. While these cytokines normally play a protective role against pathogenic microbes under physiological conditions, their excessive and prolonged release in atopic dermatitis disrupts the epidermal barrier—the skin’s first line of defense against environmental factors.

The inflammatory responses in atopic dermatitis are initially triggered by T cells, followed by other immune and tissue cells.

A research group from Japan’s Ehime University Graduate School of Medicine and Jikei University School of Medicine has been conducting fundamental studies aimed at addressing the pathogenesis of allergies by precisely regulating T-cell function. In a study published in the Journal of Allergy and Clinical Immunology, the team focused on Bach2, a protein essential for maintaining normal T-cell function.

To investigate its role in atopic dermatitis, the researchers generated three types of mouse models: mice in which Bach2 levels can be monitored using a fluorescent tag, transgenic mice with T cells expressing high levels of Bach2 (Bach2 Tg mice), and knockout mice lacking Bach2 in T cells (Bach2 KO mice).

Key findings

• T cells with low and/or intermediate levels of Bach2 accumulate in the affected areas of atopic dermatitis.
• Bach2 Tg mice do not develop atopic dermatitis, whereas Bach2 KO mice exhibit severe and prolonged (chronic) symptoms.
• Bach2 KO mice have a more fragile skin barrier, both functionally and structurally.

Bach2 levels are dynamically regulated along with T-cell status. The findings of this study suggest that precise modulation of Bach2 levels in T cells may help reduce the chronicity of atopic dermatitis, highlighting the potential for developing a novel therapeutic approach targeting Bach2 regulation in T cells.