Novel Insights into the Pathophysiology of Atopic Dermatitis

Abstract

　Atopic dermatitis (AD) is a multifactorial, chronic inflammatory skin disease that is caused by a combination of both genetic conditions and environmental factors. Mutations in the gene encoding filaggrin, which is a natural moisturizer, represent the most significant genetic factors that predispose an individual to the development of AD, as they are associated with the breakdown of the skin barrier, which leads to an increased risk of severe, early onset AD, skin infections, allergen sensitization, and food allergies, as well as the development of asthma and allergic rhinitis. In addition, abnormalities in both the adaptive and innate immune responses play a critical role in the pathogenesis of AD. The acute phase of AD is mainly characterized by the overactivation of type 2 helper T cells, while the chronic phase is characterized by the activation of type 1 helper T cells. Furthermore, environmental factors, allergens, the use of soap and detergents, and microbial infections exacerbate the breakdown of the epidermal barrier and contribute to aberrations of the immune system, further aggravating the manifestations of AD. Our understanding of AD pathophysiology will enable the better use of certain topical products, the development of new products that repair the skin barrier, and the design of new approaches for the prevention and treatment of AD.