Skin barrier protein expression

Skin barrier protein expression refers to the synthesis of key structural proteins, including filaggrin, loricrin, and involucrin, which are essential for the formation of the epidermal permeability barrier [1, 16]. These proteins are primarily produced by keratinocytes during terminal differentiation and contribute to the assembly of the cornified envelope [4, 12]. A functional skin barrier is vital for preventing transepidermal water loss and protecting the body from environmental stressors, allergens, and pathogens [1, 13]. In conditions such as atopic dermatitis and psoriasis, the expression of these proteins is significantly reduced, often due to the inhibitory effects of Type 2 cytokines like IL-4 and IL-13 or other inflammatory mediators [1, 9, 14]. This downregulation leads to barrier dysfunction, increased sensitivity, and chronic inflammation [1, 4]. Therapeutic interventions often target the restoration of skin barrier protein expression to improve clinical outcomes [2, 8]. For example, aryl hydrocarbon receptor (AhR) agonists like tapinarof directly upregulate the expression of filaggrin and loricrin [3, 11, 17]. Alternatively, biologics and small molecules that inhibit JAK-STAT signaling or specific cytokines (e.g., dupilumab) can indirectly restore barrier protein levels by alleviating inflammatory suppression [1, 9, 11]. Monitoring the expression of these proteins serves as a critical biomarker for assessing the efficacy of dermatological treatments [9, 12]. Overall, modulating skin barrier protein expression is a central strategy in managing various inflammatory and genetic skin disorders [1, 11].

Other names

Epidermal barrier protein expressionCornified envelope protein expressionSkin barrier function regulationEpidermal differentiation protein expression

Upregulation of structural proteins (e.g., filaggrin, loricrin) through the activation of regulatory transcription factors like the aryl hydrocarbon receptor (AhR) or the inhibition of suppressive inflammatory pathways such as JAK-STAT and IL-4/IL-13 signaling [1, 3, 11].