건선과 피부장벽

Abstract

The skin barrier is crucial for maintaining healthy skin by preventing loss of water and entrance of pathogenic microorganisms and irritants. Since disruption of the skin barrier induces keratinocyte proliferation, impaired barrier function is thought to be involved in the development of proliferative skin diseases, including psoriasis, which involves T helper 17 cell-related inflammation. Interestingly, skin barrier molecules such as filaggrin, loricrin, and ceramide are downregulated in psoriatic skin lesions. Moreover, the water-holding capacity and barrier recovery are also impaired in psoriatic lesions. Mice expressing activated STAT3 on keratinocytes showed disrupted barrier function and developed psoriasis-like skin inflammation. Recent studies demonstrated that defects in various skin barrier-related genes, including late cornified envelope proteins, were associated with a risk of psoriasis. In conclusion, skin barrier impairment might be closely related to psoriasis. However, further studies are required to determine whether an impaired skin barrier plays a causative role in the development of psoriasis.