Significance Atopic dermatitis (AD) is a common skin disease affecting children, but the mechanisms underlying the accompanying itch remain poorly understood. Indeed, treatments to alleviate itch in AD and the substantial morbidity it represents for patients are often unsuccessful. Here, we shed light on a form of AD associated with the loss of Tmem79 and provide insights into cellular and molecular players in this genetically driven form of the disease that has been described in mice and humans. We propose a link between this inherited form of AD and the recognized contribution of oxidative stress to this disease. Our analysis may suggest pharmacological strategies for treating patients who suffer from AD and bear mutations in Tmem79.
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Emrick et al. (2018) studied this question.
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