Atopic dermatitis (AD) is the most common chronic skin disorder among infants and young children. It is characterized by chronic relapsing eczema with itch and is caused by skin barrier dysfunction and immunological dysregulation. Scratching of the lesion site can damage the skin and increase epithelial permeability, thereby allowing large molecular weight antigens to be absorbed transcutaneously. However, a recent study demonstrated that Langerhans cells are localized close below the skin surface and extend dendrites vertically to penetrate the tight junctions (TJs) in erythematous lesions, even though the TJs were functionally intact. Therefore, epidermal barrier disruption per se is not critical for antigen uptake by Langerhans cells. In contrast, 2 critical damage-associated patterns - IL-33 and IL-1alpha - are reportedly released from damaged epithelial cells. Dendritic cells activated by IL-33 and thymic stromal lymphopoietin (TSLP) (induced by IL-1 alpha) express MHC class II and costimulatory molecules and facilitate naive T cell differentiation into IL-5- and IL-13-secreting Th2 cells. IL-33 and TSLP also activate type 2 innate lymphoid cells, induce large amounts of IL-5 and IL-13, and participate in the pathogenesis of AD. Primary prevention and proactive treatment of AD are critically important for preventing epicutaneous sensitization in AD patients. However, future studies are required to elucidate the most beneficial primary prevention strategies, including the indicated patient cohort and the timing and method of their application.
All Science Journal Classification (ASJC) codes
- Pediatrics, Perinatology, and Child Health
- Immunology and Allergy
- Pulmonary and Respiratory Medicine