Atopic Dermatitis: The Relationship Between Immune Mediators and Skin Lipid Barrier.

Atopic dermatitis (AD) is a chronic inflammatory skin disease that is prevalent worldwide with complex etiology. Skin barrier defects and abnormal immune activation are crucial in the occurrence and development of AD. In the classic model of the skin barrier, lipids are essential for the formation and maintenance of this barrier as a "mortar" component. However, abnormally activated immune responses promote the lipid barrier deficiency through the secretion of various types of immune mediators directly or indirectly. In this review, we first introduce the skin lipid barrier (SLB) under both normal and abnormal conditions, highlighting the contributions of lipids derived from keratinocytes and sebaceous glands (SGs). Subsequently, the relationships between the immune mediators of Th1, Th2, Th17, Th22, and other types (adipokines, prostaglandins, leukotrienes) and SLB are elaborated in turn. Finally, the therapies for restoring SLB to treat AD are summarized, with a focus on the restoration effect of dupilumab on SLB. We hope that this review will offer a comprehensive perspective for understanding the pathogenesis of lipid metabolism disorders and SLB deficiency caused by immune mediators in AD. It also aims to provide guidance for further research on targeting inflammatory mediators to restore SLB.