1. ¹University of California, San Francisco School of Medicine, San Francisco, California, USA
2. ²National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA

Correspondence: Dr Julia A. Segre, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, 49 Convent Drive, Room 4A26, Bethesda, Maryland 20892, USA. E-mail: jsegre@nhgri.nih.gov

Abstract

Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disorder that affects approximately 15% of children in the United States. A complex disorder, AD is characterized by both skin barrier impairment and immunologic abnormalities, including decreased innate immune function and a polarized adaptive immune response. Mouse models have demonstrated the complex interdependence of immune cell–keratinocyte interactions and teased apart gene–environment relationships in a controlled setting. In this issue, Nagelkerken et al. present a mouse model with transgenic expression of apolipoprotein C1 that disrupts the skin lipid barrier and manifests many hallmark features of AD.