Innate immunity, allergy and atopic dermatitis

Abstract

We review here the recent discoveries in innate immunity that shed light on the pathophysiology of atopic dermatitis. The mechanisms that promote the enhanced susceptibility to cutaneous infections in atopic dermatitis are complex interactions among several factors. They include skin barrier dysfunction, reduced skin lipid content, and abnormalities of the innate immune response. Some of the innate immune defects observed in atopic dermatitis are primary defects, such as epithelial barrier defects and defects in signaling or expression of innate receptors. Others may be secondary to the effects of the adaptive immune response. For example, deficiencies in antimicrobial peptides may be due to the overexpression of T helper 2 cytokines such as interleukin-4 and interleukin-13. However, how all components interact with each other remains to be fully investigated. To break this vicious circle, a multiprolonged approach directed at healing or protecting the skin barrier and addressing the immune dysregulation is necessary to improve and control the disease.