Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by pruritus, dry and leathery skin, and intense itching. It affects 20% of children and 1-3% of adults, with a bimodal curve peaking in early childhood and middle-aged adulthood. AD is part of the "atopic triad" along with allergic rhinitis and bronchial asthma, and recent studies suggest a sequential development of these conditions. AD can be classified based on age of onset, with very early onset (three months to two years), early onset (two to six years), childhood onset (six to fourteen years), adolescent onset (fourteen to eighteen years), adult-onset (twenty to sixty years), and very late onset (over sixty years). Diagnosis relies on clinical observations, with minor criteria including flexural dermatitis, dry skin, asthma, and rash before two years of age. The skin's immune system plays a crucial role in AD, with innate and adaptive immune responses contributing to barrier dysfunction and inflammation. Key players include keratinocytes, Langerhans cells, dendritic cells, and various immune cells. Genetic factors, such as mutations in the filaggrin gene, and environmental triggers, like exposure to irritants and allergens, contribute to AD pathogenesis. The "hygiene hypothesis" suggests that exposure to pathogens may protect against AD, while air pollution and industrialization can exacerbate the condition. Understanding the interplay between genetic predisposition and environmental factors is essential for developing effective prevention and treatment strategies.Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by pruritus, dry and leathery skin, and intense itching. It affects 20% of children and 1-3% of adults, with a bimodal curve peaking in early childhood and middle-aged adulthood. AD is part of the "atopic triad" along with allergic rhinitis and bronchial asthma, and recent studies suggest a sequential development of these conditions. AD can be classified based on age of onset, with very early onset (three months to two years), early onset (two to six years), childhood onset (six to fourteen years), adolescent onset (fourteen to eighteen years), adult-onset (twenty to sixty years), and very late onset (over sixty years). Diagnosis relies on clinical observations, with minor criteria including flexural dermatitis, dry skin, asthma, and rash before two years of age. The skin's immune system plays a crucial role in AD, with innate and adaptive immune responses contributing to barrier dysfunction and inflammation. Key players include keratinocytes, Langerhans cells, dendritic cells, and various immune cells. Genetic factors, such as mutations in the filaggrin gene, and environmental triggers, like exposure to irritants and allergens, contribute to AD pathogenesis. The "hygiene hypothesis" suggests that exposure to pathogens may protect against AD, while air pollution and industrialization can exacerbate the condition. Understanding the interplay between genetic predisposition and environmental factors is essential for developing effective prevention and treatment strategies.