Atopic dermatitis (AD) is a chronic inflammatory skin disease that most commonly occurs during early infancy and childhood and is characterized by a chronically relapsing course where symptoms of AD are ameliorated and aggravated repeatedly. Although the pathogenesis of AD is not fully understood, it has been reported that it is associated with multiple immunologic abnormalities.1,2 The most prominent findings of immune dysfunction are the high level of immunoglobulin E (IgE) in peripheral blood and increased IgE production by B cells. In AD, T helper 2 (Th2) cells are mainly activated and then secrete interleukin-4 (IL-4), interleukin-5 (IL-5) and interleukin-10 (IL-10).1, 3, 4
Symptoms of AD induced by signal transduction pathways of IgE, IL-4, IL-5 or IL-10 are associated with inflamed skin damage as well as skin dryness. Accordingly, the generally accepted prescription includes moisturizers and topical steroids that maintain a level of moisture in the skin and suppress inflammatory reaction, respectively. However, treating AD over time with topical steroid hormones has been known to induce adverse side effects.5 In addition, nonsteroid therapeutic treatments including cyclosporin A and tacrolimus have been reported to induce cutaneous T cell lymphoma, fever, extreme rises in serum alkaline phosphatase in children, enhanced irritation and relapsing Kaposi’s varicelliform eruption.6–10 Therefore, much recent work has focused on the development of therapeutic agents that maximize anti-inflammatory effects while minimizing side effects.
