Selective Ablation of Ctip2/Bcl11b in Epidermal Keratinocytes Triggers Atopic Dermatitis-Like Skin Inflammatory Responses in Adult Mice

The study explored the role of Ctip2/Bcl11b in epidermal keratinocytes by selectively deleting it in adult mice, leading to atopic dermatitis-like skin inflammation characterized by alopecia, pruritus, and immune cell infiltration. The absence of Ctip2 resulted in increased expression of Th2-type cytokines and chemokines, such as TSLP, CCL17, IL13, and IL4, which are crucial in inflammatory skin diseases. The findings highlighted Ctip2's essential role in maintaining skin barrier function and suppressing inflammatory responses, suggesting its potential involvement in atopic dermatitis pathogenesis and providing a model for further research into therapeutic strategies.