Up to 10 percent of normal individuals carried mutations
in the filaggrin gene in these northern nations, in contrast to much lower mutation rates in southern European, Asian and African populations.
Infants were also screened for mutations
in the filaggrin (FLG) gene, which codes for a key skin barrier protein.
Not exact matches
A new report by researchers
in the Perelman School of Medicine at the University of Pennsylvania found that loss - of - function mutations to
Filaggrin - 2 (FLG2), a gene that creates a protein responsible for retaining moisture and protecting the skin from environmental irritants, were associated with atopic dermatitis
in African American children.
Previous studies have shown than those of African descent do not usually carry a mutation to the
filaggrin gene (FLG) that has been associated with the risk of onset and persistence of AD
in those of European and Asian ancestry.
Filaggrin, a key protein
in skin barrier function, is deficient
in adults.
The deficit of
filaggrin has been blamed for the poor skin barrier
in eczema.
In contrast to adults, however, the skin of young children with eczema was found to have plenty of
filaggrin, despite its poor barrier function and skin thickening that is comparable to skin of adults with eczema.
He recently has focused on a specific skin - barrier protein called
filaggrin, which is broken down into a molecule called urocanic acid — the most potent absorber of UVB light
in the skin, according to Elias.
Moreover, higher
filaggrin mutation rates, which result
in a loss of urocanic acid, correlated with higher vitamin D levels
in the blood.
Filaggrin plays a critical role
in the skin barrier integrity.