期刊名称：Annals of Agricultural and Environmental Medicine
印刷版ISSN：1232-1966
电子版ISSN：1898-2263
出版年度：2007
卷号：14
期号：02
页码：195-195
出版社：Institute of Agricultural Medicine in Lublin
摘要：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 (= fi lament-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 fi laggrin expression
in skin. Half or more of children with moderate to severe AE carry FLG mutations.
Moreover, fi laggrin loss-of-function mutations predispose to phenotypes involved in the
atopy march. The altered skin structure and a defi ciency 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 proinfl ammatory cytokines and chemokines
with activation of T lymphocytes, dendritic cells, macrophages, keratinocytes, mast cells,
and eosinophils which lead to the skin infl ammatory 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.
