Atopic eczema (AE) is a multifactorial
skin disease caused by a variety of factors such as genetic conditions, alterated skin structure, immunologic deviations and environmental factors, among others. There are two main subtypes of AE, i.e. the
IgE-associated ("
atopic eczema") and the non-
IgE-associated type ("nonatopic
eczema") with different prognosis concerning the development of
respiratory diseases ("atopy march"). Recently, it was demonstrated that
Filaggrin (=filament-aggregating
protein, FL) is a major gene for
atopic eczema.
Filaggrin binds to and aggregates the
keratin cytoskeleton in the epidermis. Homozygous FLG mutation leads to complete loss of
filaggrin expression in skin. Half or more of children with moderate to severe AE carry FLG mutations. Moreover,
filaggrin loss-of-function mutations predispose to phenotypes involved in the atopy march. The altered skin structure and a deficiency in
antimicrobial peptides favour colonization with Staphylococcus aureus and yeasts (Malassezia sp.). Sensitization to the yeast occurs almost exclusively in AE patients. S. aureus
enterotoxins with superantigenic activity stimulate activation of T cells and macrophages. So far, AE skin lesions are orchestrated by the local tissue expression of proinflammatory
cytokines and
chemokines with activation of T lymphocytes, dendritic cells, macrophages, keratinocytes, mast cells, and eosinophils which lead to the skin inflammatory responses. From the therapeutic point of view, besides
emollients and local
corticosteroids, topic
immunomodulatory drugs (
tacrolimus and
pimecrolimus) have substantially improved the treatment of AE.