The recent identification of loss-of-function mutations in the structural protein filaggrin as a
widely replicated major risk factor for eczema sheds new light on disease mechanisms in
eczema, a disease that had heretofore largely been considered to have a primarily
immunologic etiopathogenesis. The filaggrin gene (FLG) mutation findings are consistent
with a recently proposed unifying hypothesis that offers a mechanistic understanding of
eczema pathogenesis synthesizing a heritable epithelial barrier defect and resultant …