IL-17 downregulates filaggrin and affects keratinocyte expression of genes associated with cellular adhesion.

摘要: Atopic eczema and psoriasis are common skin diseases. While it is well established that the pathogenesis of these diseases varies, both characterized by impairment in epidermal barrier function abnormal IL-17 expression peripheral blood. Recent findings indicated filaggrin essential during formation its insufficiency underlies atopic eczema. Filaggrin downregulation has also been reported psoriasis. It clear Th1/Th2 bias influences protein, but an analysis effects interleukin-17 (IL-17) on protein profilaggrin-processing enzymes not yet reported. In addition, effect cytokine components functional barrier, tight junctions adhesion/desmosomal proteins, elucidated. Keratinocytes were exposed to interleukin-17A, microarray was performed. level assessed western blot. We have observed a significant decrease profilaggrin mRNA interleukin-17A-exposed cultures (P = 0.008). Expression processing altered, indicating indirect production/degradation. Moreover, many genes involved cellular adhesion decreased. A at detected blot immortal primary keratinocytes. Gene ontology changes keratinization, differentiation cornified envelope. conclude IL-17A downregulates important for which could affect formation. This potentially contributes dysfunction become possible therapeutic target.