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Inflammatory-Driven Depletion of Filaggrin Proteins

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Filaggrin

Abstract

Filaggrin has become the major research focus within the field of skin barrier abnormality over the last 5–10 years. Null mutations in the (pro)-filaggrin gene (FLG) have been shown to be a major risk factor for the development of atopic dermatitis, a disease in which one of the hallmarks is a decreased skin barrier function. However, only between 30 and 40 % of the patients suffering from atopic dermatitis carry the mutation, and yet all of them have a barrier defect, and patients suffering from other skin diseases such as contact dermatitis and psoriasis also have a decreased skin barrier function. From the studies of keratinocyte cell cultures and animal models, it has become clear that inflammation in itself is actually able to induce downregulation of filaggrin expression on transcriptional and translational levels and decrease processing of pro-filaggrin into filaggrin. The literature on this subject is concentrated on the effect of inflammatory cytokines but is still very scarce. More research into this area may offer new insight into the pathogenesis of reduced skin barrier function in inflammatory skin diseases, and it may lead to new principles of treatment in these skin diseases.

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Vestergaard, C., Deleuran, M.S. (2014). Inflammatory-Driven Depletion of Filaggrin Proteins. In: Thyssen, J., Maibach, H. (eds) Filaggrin. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-54379-1_4

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