Abstract. It has been recognized that atopic dermatitis (AD) involves allergen-driven Th2 cell polarization. In patients with AD, cytokines induce allergic inflammatory responses and subsequently enhance IgE production. Recent reports revealed that a reduced barrier function as well as altered immunity are fundamental to the development of AD because barrier disruption due to aberrant filaggrin expression is a pathological factor. However, although recent studies have improved our understanding of the pathogenesis of AD, the overall pathophysiology remains elusive. I herein discuss it based on the natural history of AD.Keywords: atopic dermatitis, nonatopic dermatitis, barrier dysfunction, filaggrin, IgE autoantibody, allergic inflammation
Clinical manifestations of atopic dermatitis (AD)AD is a chronic inflammatory skin disease characterized by itchy dermatitis and susceptibility to cutaneous bacterial, viral, and fungal infections. Other hallmarks of AD are a defect in the barrier function, causing dry skin, and IgE-mediated sensitization to food and environmental allergens (1). The clinical manifestations of AD vary with age. There are three stages: 1) in infancy, the first eczematous lesions usually appear on the cheeks and scalp; 2) in childhood, lesions involve flexures and the extensor aspects of the limbs; and 3) in adolescence and adulthood, lichenified plaques affect the flexures, face, and neck. In each stage, itching worsens the skin lesions and impairs the patient's quality of life.The prevalence of AD has markedly increased during the past three decades. A total of 45% of all cases of early-onset AD begin within the first 6 months of life, 60% begin during the first year, and 85% before 5 years of age. More than 50% of the children affected up to 2 years of age do not show any signs of IgE-sensitization, but they become sensitized during the course of the disease (2). Up to 70% of these children undergo spontaneous remission before adolescence.
Immunopathology of AD