UC San Diego

Atopic dermatitis (AD) is a chronic inflammatory skin disease that features eczematic skin lesions, pruritus (itch), spongiosis (skin edema) and is triggered by a complex genetic and environmental background. The deletion of epidermal caspase-8 in mouse shares similarities with the AD pathology and a rare genetic cause of AD. This caspase-8 KO mouse model display skin barrier dysfunction, recruitment of immune/inflammatory cells, gene expression of genetic signatures related to AD, elevated immunoglobulin levels and trans-epidermal water loss which are all very similar to the pathophysiology of AD. Using this mouse model, we have identified proteases (MMPs - matrix metalloproteases) that may play a role in the skin barrier dysfunction and play a possible mechanism in spongiosis.