Epidermis-Specific Ablation of Claudin-1 in Adult Mice Demonstrates the Essential Role of a Tight Junction Barrier in Skin Homeostasis

The study demonstrated the essential role of tight junctions (TJs) in skin homeostasis by using tamoxifen-inducible epidermis-specific claudin-1 knockout mice. The absence of claudin-1 led to TJ barrier leakage, which activated Langerhans cells without initially affecting the stratum corneum (SC) or increasing water loss. By day 18, however, the TJ barrier leakage resulted in SC barrier defects, increased water evaporation, and trans-epidermal water loss, along with symptoms such as erythema, scales, abnormal sebum secretion, partial hair loss, and scratching behaviors. These findings suggested that TJ barrier leakage could induce SC barrier defects and skin inflammation, highlighting a potential mechanism for the development of atopic dermatitis.