The new findings of the international team of researchers led by Prof. Eli Sprecher, are expected to change the therapeutic approach in allergic diseases.
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The prevalence of allergic diseases, such as atopic dermatitis, is steadily increasing over the past decade for reasons which are not entirely known. For years, it had been thought that atopy results from a primary dysfunction of the immune system. This notion resulted in numerous attempts to treat atopic dermatitis through varied strategies all aimed at attenuating the immune system activity at the cost of often severe side effects such as an increase in the prevalence of infectious complications.
The skin barrier
More recently, however, immunological abnormalities have been suspected to occur in allergic diseases as the mere consequence of a primary defect residing within the skin barrier. This barrier is in fact a functional entity located in the upper layers of the skin; it separates us from our environment and makes sure essential nutrients and proteins are kept within the body, while unwanted intruders, including allergens, are prevented to gain access to the inside of our body. The skin barrier functionality has been shown to be dependent upon the presence within our cells of several proteins such as filaggrin, whose absence is considered as a major risk factor for atopic dermatitis.
Now, an international team of researchers led by Prof. Eli Sprecher at the Department of Dermatology at the Tel Aviv Sourasky Medical center and Tel Aviv University, Israel and Prof. Kathy Green from Northwestern University, USA report in the prestigious journal Nature Genetics, that key to the proper function of the barrier are small but complex protein units, called desmosomes.
Liat Samuelov who co-led the project with Ofer Sarig in Tel Aviv comments: “Desmosomes are responsible for ensuring cell-cell adhesion within all layers of the skin. We found out that a critical component of the desmososmes called desmoglein 1 is missing in the skin of patients affected by a life-threatening form of allergic skin disease called SAM syndrome (Severe dermatitis, Allergy, and Metabolic wasting). Sarig adds: “The disease is caused by poorly functional bonds between cells located in the upper part of the skin. This is apparently enough for foreign proteins to move across the skin barrier and elicit an exaggerated immune response. Even more interestingly, when we studied isolated cells from the patients, these were found to secrete numerous mediators of allergy. Thus our data call into question the role of the immune system in allergic processes, with obvious implications for the development of new therapeutic strategies in atopic dermatitis”.