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Filaggrin inhibits generation of CD1a neolipid antigens by house dust mite–derived phospholipase

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Science Translational Medicine  10 Feb 2016:
Vol. 8, Issue 325, pp. 325ra18
DOI: 10.1126/scitranslmed.aad6833

Bringing atopic dermatitis up to scratch

Targeted therapies are transforming medicine, but complex diseases such as atopic dermatitis are difficult to target. Now, Jarrett et al. report a mechanism that links two contributors to atopic dermatitis pathogenesis—cutaneous inflammation and barrier dysfunction. They found that house dust mite allergen phospholipase (PLA2) can induce neolipid antigens in human skin. These antigens can then be presented by the nonclassical MHC family member CD1a to CD1a-restricted T cells, which contribute to inflammation. The skin barrier protein filaggrin can inhibit PLA2 and decrease this inflammation. Indeed, individuals with filaggrin mutations experience severe atopic dermatitis. These data suggest that barrier dysfunction and inflammation may be linked, and support PLA2 as a target for atopic dermatitis.

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