Abstract
There is an increasing number of experimental, genetic and clinical evidence of atopic dermatitis expression as a pre-condition for later development of other atopic diseases such as asthma, food allergy and allergic rhinitis. Atopic dermatitis is a heterogeneous, recurrent childhood disease, also present in the adult age. It is increasingly attributed to systemic features and is characterized by immunological and skin barrier integrity and function dysregulation. To maintain the protective function of the skin barrier, in particular the maintenance of pH, hydration and antimicrobial functions, the filaggrin, among others, plays a significant role. Filaggrin is a multifunctional, histidine-rich, insoluble protein. The lack of filaggrin is associated with various cutaneous (e.g. ichthyosis vulgaris, allergic contact dermatitis) and non-cutaneous (e.g. diabetes, inflammatory conditions of the gastrointestinal tract) diseases and may be a result of genetic, immunological factors combined with environmental factors. In this review we summarised (emphasized) recent findings in understanding the role of filaggrin in atopic dermatitis and other diseases, participants in the atopic march.
Highlights
The term atopy, which was first coined by Coca and Cooke in 1923, represents immunoglobulin (Ig) E-mediated type I hypersensitivity reactions [1]
We focus on the FLG molecule and its importance in maintaining normal skin barrier function and on current knowledge of the significance of FLG deficiency in diseases associated with atopic march
It is indisputable that the interactions between impaired epidermal barrier and dysregulation of the innate and adaptive immune system, in association with environmental risk factors, are involved in pathogenesis of atopic dermatitis (AD)
Summary
The term atopy, which was first coined by Coca and Cooke in 1923, represents immunoglobulin (Ig) E-mediated type I hypersensitivity reactions [1]. The most investigated causes of the epidermal skin barrier impairment in AD, as the initiator of atopic march, are a lack of filaggrin (FLG) associated with decrease of ceramide and significant activation of epidermal proteases [14]. We focus on the FLG molecule and its importance in maintaining normal skin barrier function and on current knowledge of the significance of FLG deficiency in diseases associated with atopic march. The TSLP (thymic stromal lymphopoietin), a type I cytokine produced by keratinocytes through the protease-activated receptor-2 (PAR-2) mediated nuclear factor kappa B (PAR-2/NF-kB) pathway, has the greatest significance. This cytokine has an essential role in the initiation of allergic inflammation in the skin.
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