Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disorder affecting up to 20% of children and adults. Underlying the pathogenesis of AD are Th2 cytokines interleukin (IL)-4 and IL-13, secreted by immune cells. In addition, epidermal barrier disturbances add to the exacerbation of AD. Recent studies identify an important role for epidermal tight junction (TJ) barrier disruption in the pathogenesis of AD. Our laboratory previously demonstrated that loss of EPHA2, a receptor tyrosine kinase (RTK), led to the abrogation of epidermal TJ barrier formation and function.
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