Abstract
Atopic dermatitis (AD) patients suffer from increased susceptibility to cutaneous viral infections and diminished epidermal barrier function, including defects in TJ integrity and reduced claudin-1 (CLDN1) expression. To understand the role of CLDN1 in epidermal viral infections, we generated keratinocytes (KC) lacking CLDN1 using CRISPR/Cas9 technology. CLDN1 knockout (CLDN1KO) KC were evaluated for barrier function, differentiation, and susceptibility to vaccinia virus (VV), the causative agent of the life-threatening, AD-related complication, eczema vaccinatum.
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