Atopic dermatitis is a chronic inflammatory skin disease that causes significant morbidity in affected individuals. It is characterized by dysregulated immune responses that consist of an increased systemic Th2 response and a combination of Th2 and Th1 responses in the skin lesions. In this article, we review factors that contribute to these abnormal responses, including key effector cells of the immune system, chemokines, defective skin barrier, genetic predisposition, and environmental triggers. Understanding these pathomechanisms may improve our current therapies for atopic dermatitis.