Article

Clinical Reviews in Allergy & Immunology

, Volume 47, Issue 2, pp 193-218

Molecular Biology of Atopic Dermatitis

  • Zhanglei MuAffiliated withDepartment of Dermatology, Peking University People’s Hospital
  • , Yan ZhaoAffiliated withDepartment of Dermatology, Peking University People’s Hospital
  • , Xiaojing LiuAffiliated withDepartment of Dermatology, Peking University People’s Hospital
  • , Christopher ChangAffiliated withDivision of Allergy and Immunology, Thomas Jefferson University Email author 
  • , Jianzhong ZhangAffiliated withDepartment of Dermatology, Peking University People’s Hospital Email author 

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Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease with specific genetic and immunological mechanisms. The rapid development of new techniques in molecular biology had ushered in new discoveries on the role of cytokines, chemokines, and immune cells in the pathogenesis of AD. New polymorphisms of AD are continually being reported in different populations. The physical and immunological barrier of normal intact skin is an important part of the innate immune system that protects the host against microbials and allergens that are associated with AD. Defects in the filaggrin gene FLG may play a role in facilitating exposure to allergens and microbial pathogens, which may induce Th2 polarization. Meanwhile, Th22 cells also play roles in skin barrier impairment through IL-22, and AD is often considered to be a Th2/Th22-dominant allergic disease. Mast cells and eosinophils are also involved in the inflammation via Th2 cytokines. Release of pruritogenic substances by mast cells induces scratching that further disrupts the skin barrier. Th1 and Th17 cells are mainly involved in chronic phase of AD. Keratinocytes also produce proinflammatory cytokines such as thymic stromal lymphopoietin (TSLP), which can further affect Th cells balance. The immunological characteristics of AD may differ for various endotypes and phenotypes. Due to the heterogeneity of the disease, and the redundancies of these mechanisms, our knowledge of the pathophysiology of the disease is still incomplete, which is reflected by the absence of a cure for the disease.

Keywords

Molecular biology Atopic dermatitis Eczema Filaggrin Cathelicidin Atopy Atopic march IgE Thymic stromal lymphopoeitin Tumor necrosis factor-alpha