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Available from: Alan Irvine, Jan 30, 2015
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    • "A critical link between the barrier defect in AD patients with FLG mutations and Th2 polarization could be explained in part by enhanced allergen penetration through the damaged epidermis accompanied by increased production of thymic stromal lymphopoietin (TSLP) by keratinocytes leading to a Th2-type milieu.46 Importantly, patients with FLG gene mutations are at an increased risk for developing asthma, but only in the context of having AD, pointing to the importance of allergic sensitization through a damaged skin barrier.44,47,48 Conversely, AD patients with more polarized Th2-type disease with allergies and asthma and increased biomarkers including serum IgE, TSLP and cutaneous T cell-attracting chemokine were also more likely to have severe skin disease complicated by eczema herpeticum (EH), Staphylococcus aureus or molluscum infections.49 "
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    ABSTRACT: Atopic dermatitis (AD) is a complex disease that affects up to 20% of children and impacts the quality of patients and families in a significant manner. New insights into the pathophysiology of AD point to an important role of structural abnormalities in the epidermis combined with immune dysregulation. Filaggrin (FLG) is synthesized as a large precursor, profilaggrin, and is expressed in the upper layers of the epidermis. FLG plays a critical role in the epidermal barrier, and FLG mutations cause abnormal epidermal function. FLG mutations are strongly associated with early-onset, and persistent severe AD. In addition, FLG deficiency in the epidermis is related to allergic sensitization and asthma. The basic skin care including repair and protection of the skin barrier with proper hydration and topical anti-inflammatory therapy is important to control the severity of skin disease in patients with AD.
    Full-text · Article · Jan 2012 · Allergy, asthma & immunology research
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  • No preview · Article · May 2008 · Journal of Allergy and Clinical Immunology
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