An important feature of the inflammation in atopic dermatitis (and in the other ‘atopic’ disorders, such as asthma) is the overproduction of ‘bad’ cytokines, such as interleukin 4 (IL-4), by a subgroup of Th2-type lymphocytes. After secretion from Th2 cells, IL-4 percolates up into the epidermis where it decreases the production of both lipids and proteins that are critical for normal barrier function (see our recent series of articles on atopic dermatitis for more information on the link between the barrier and Th2 cytokines).
One would anticipate, therefore, that if one could block the actions of IL-4, the dermatitis might improve. This is just what Lisa Beck’s group at the University of Rochester reported at the recent IID meeting in Edinburgh. They presented the results of a Phase I clinical trial, using a monoclonal antibody, dupilumab (REGN668/SAR233693), directed against a portion of the IL-4 molecule in adult patients with severe atopic dermatitis. When administered in only 4 weekly subcutaneous or intravenous doses, they observed both rapid and sustained improvement in severity of the dermatitis and symptoms of itch in ~70 and 45% of patients, respectively. Equally encouraging was the minimal evidence for significant toxicity.
Bottom Line: While larger clinical trials still need to be performed before this product will become commercially available, these promising results provide hope that a specific, well tolerated and effective systemic treatment for more severe atopic dermatitis may not be too far off.