Tolerance induction in atopic skin
Healthy skin is able to maintain optimal immunological balance, despite being colonised with numerous bacteria species, and exposed to constant challenges from the environment (dust, chemicals, sunshine, etc…).
In contrast, atopic skin is constantly inflamed. This study aims to investigate how are immune responses regulated in patients with atopic dermatitis
What do we know about atopic skin?
Atopy is defined as a personal or familial propensity to produce IgE antibodies and sensitization in response to environmental triggers. It has been observed, that patients with atopy often develop a sequence of progressing atopic manifestations, including atopic dermatitis, food allergy, allergic rhinitis, and asthma (so called “atopic march”). The cutaneous manifestations of atopy often represent the beginning of the atopic march. On the basis of several longitudinal studies, approximately half of AD patients will develop asthma, particularly with severe AD, and two thirds will develop allergic rhinitis. Epicutaneous sensitization has been thought to be responsible, with subsequent migration of sensitized T cells into the nose and airways, causing upper and lower airway disease.
Atopic skin has been shown to be different to healthy skin in several important aspect:
- Impaired barrier
Structure of atopic skin is more permeable – meaning more allergens can penetrate through skin, and more water can transpire
- Aberrant immune responses
Atopic skin have been shown to react differently to allergens, and is often a site of ongoing allergic inflammation
- Allergic inflammation
Numerous “allergic” cell types infiltrate atopic skin, and release pro-inflammatory mediators, causing itch, rash, and eczema.
Our study aims to dissect how allergen handling is altered in atopic skin, and what we can do to bring it back to healthy.