Thus, genetic evidence suggests that epithelial factors have important roles in the development of AD and its TH2 cell–related comorbidities, while a predisposition to TH17 responses and dysregulation of inflammatory signaling in immune and nonimmune components, such as keratinocytes, contribute to the development of psoriasis. Clinical and experimental evidence therefore indicates that the inflammatory loop at the EIME determines the key features of AD and psoriasis. We describe the details of the inflammatory loop at the EIME in each disease in the following sections