Atopic dermatitis (AD) is a chronic, recurrent, pruritic, inflammatory skin disease that severely affects the quality of life of patients and their families. The disease is associated with genetic allergies and is often associated with skin barrier dysfunction. The disease usually begins in infancy, and some data show that about 50% of all patients develop the disease before the age of 1 year. The prevalence of AD can be as high as 10%-20% in developed countries, and epidemiological surveys in China also show an increasing trend in the incidence of this disease, for example, in 2000, the epidemiological survey in China showed that the total prevalence of school-age adolescents (6-20 years old) was 0.70% [1], and in 2004, the prevalence of urban preschool children (1-7 years old) was 2.78% [2]. The incidence of AD in general decreases with age and the disease may gradually decrease. The etiology and pathogenesis of atopic dermatitis are very complex and have not been fully understood. Genetic, environmental, and biological factors are closely related to the disease [3]. Children of parents with a history of genetic allergies have a significantly increased chance of developing the disease, but genetics is not the only determining factor. Environmental factors, especially the degree of industrialization, urban living, standard of living and changes in lifestyle are important risk factors for the development of AD. Among allergic factors, diet such as milk, eggs and seafood have an influence on the development of AD, especially in those with severe disease in infancy and early childhood. Dust mites, house dust mites, and pollen may be important airborne allergens. Non-allergic factors such as irritants or detergents that disrupt the skin barrier, scratching, microbial colonization (e.g., Staphylococcus aureus and Malassezia furfur), and psychological factors (e.g., stress, anxiety, depression) also play an important role in the pathogenesis [3,4]. The exact pathogenesis of AD is not known. It is generally believed that it is caused by dysfunction of the body’s skin barrier or direct dysregulation of the body’s immune response in response to certain genetic background and/or environmental factors, leading to allergic or non-allergic inflammatory reactions. Skin barrier dysfunction creates conditions for local sensitization of allergens or microbial colonization, which is an important basis for triggering or aggravating skin inflammation. The development of atopic dermatitis involves both immune and non-immune aspects. Immune-mediated inflammation involves several components, including the presentation of allergens by Langerhans cells and cutaneous dendritic cells, dysregulation of Th1/Th2 balance and regulatory T cell dysfunction, involvement and amplification of the inflammatory response process by eosinophils and specific IgE, and the production of cytokines and inflammatory mediators by keratinogenic cells involved in the inflammatory response. In recent years it has been noted that non-immune factors such as neuro-endocrine factors or abnormal physiological and pharmacological mediator responses are also involved in the formation of skin inflammation [3-5]. The above inflammatory processes are an important basis for the therapeutics of atopic dermatitis.