Figure 4.

Model for the etiology of AE. (i) Skin irritants increase ATP release in the skin in Zn deficiency, due to increased ATP release by KCs, impaired ATP hydrolysis by LCs, and impaired ENPP activity. (ii) Increased ATP release induces severe and prolonged ICD via aberrant chemokine production by KCs and neutrophil-mediated skin inflammation. Histologically, cutaneous lesions in AE and ICD lesions in ZD mice demonstrate common histological features, such as subcorneal vacuolization and epidermal pallor.