Recent advances in atopic dermatitis

Abstract

The prevalence and disease burden of atopic dermatitis (AD) is substantial. AD causes significant impairment in quality of life. It is also associated with mental disorders as well as cardiovascular diseases. Many factors including race, environment, skin barrier dysfunction, immune regulatory abnormalities, and microbiome have been reported to affect the pathophysiology of AD. A variety of cell types including Th2, Th17, Th22, and type 2 innate lymphoid cells contribute to AD. Cytokines from these immune cells cause abnormal epidermal differentiation and skin barrier dysfunction. Moreover, microbial dysbiosis and deficiency of antimicrobial peptides result in Staphylococcus aureus infection. Recently, new drugs have been successfully launched to target polarized immune pathways that lead to moderate-to-severe AD.

Figure 1.. Pathophysiology of atopic dermatitis.

Epidermal barrier defects, cutaneous dysbiosis, and immune dysregulation play important roles in the pathophysiology of AD. TSLP, IL-25, IL-33, and ILC2 induce production of Th2, Th17, and Th22 cytokines directly or indirectly. TSLP activates antigen presenting cells, dendritic cells, basophil, and ILC2 to produce Th2 and Th17 cytokines. IL-26 from Th17 cells induces production of IL-4, IL-13, IL-17A, and IL-33. Abbreviations: AMPs, antimicrobial peptides; ILC2, type 2 innate lymphoid cell; Th2, T helper type 2; Th17, T helper type 17; Th22, T helper type 22; TJ, tight junction; TSLP, thymic stromal lymphopoietin.