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Dust Mites Help Identify Pathway to Treat Atopic Dermatitis

Atopic dermatitis (AD) has complex genetic and environmental susceptibility factors. However, previous research has shown that null mutations in the gene encoding filaggrin (a filament-associated protein that binds to keratin fibers in epithelial cells) are associated with moderate to severe clinical disease. Filaggrin is involved with skin barrier, cutaneous pH regulation, hydration, and antimicrobial protection. One hypothesis is that filaggrin disruption allows immune stimuli to enter the skin and activate immune responses. However, there has been considerable debate about the relative roles of barrier function and cutaneous inflammation in AD pathogenesis.

About 80% of people with AD have elevated serum immunoglobulin E (IgE), which recognize proteins that derive from common environmental allergens such as the house dust mite (HDM). A recent study published in Science Translational Medicine sought to identify a pathway that links two contributors to atopic dermatitis pathogenesis—cutaneous inflammation and barrier dysfunction. The researchers obtained skin and blood samples from individuals with atopic dermatitis and healthy controls, and then exposed the samples to house dust mite allergen phospholipase (PLA2). They observed that HDM allergen generates neolipid antigens in skin. These antigens can then be presented by the nonclassical MHC family member CD1a to CD1a-restricted T cells, which contribute to inflammation.  Filaggrin was shown to inhibit the phospholipid activity and decreased the inflammation caused by the allergen.  These data suggest that barrier dysfunction and inflammation may be linked, and support PLA2 inhibition as a targeted therapeutic approach for atopic dermatitis.

Byline: Martha L. Sikes, MS, RPh, PA-C

Posted: March 15, 2016

Source: Science Translational Medicine
Adapted from the original article.

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