[Immune mechanisms of atopic dermatitis]

The syndrome of atopy consists of three major clinical entities, i.e., allergic rhinoconjunctivitis, allergic asthma and atopic dermatitis, and is usually associated with elevated serum IgE levels. Whereas the pathogenetic role of IgE is clearly established in the case of allergic rhinoconjunctivitis and allergic asthma, the occurrence of atopic dermatitis cannot be easily explained by hyperimmunoglobulinemia E. Atopic dermatitis clinically presents as eczematization of certain predisposed (mostly flexural) areas of the skin. The clinical and histopathological picture, as well as the emergence kinetics of atopic eczema, roughly follow the criteria of delayed type (type IV) immune reactions. It is at present unclear whether the type I-like and the type IV-like allergic reactions of atopy are events occurring independently of each other or, alternatively, are pathogenetically linked to each other. Recent data suggest that in contrast to allergic contact dermatitis where Th 1-like T cells producing interleukin (IL)-2 and interferon (IFN)-gamma are the cells eliciting the lesions, the cellular infiltrate of atopic dermatitis lesions is dominated by Th2 cells capable of producing IL-4 and IL-5. Consequently, two clinical findings of atopic disorders are explicable by the observed Th2 cytokine secretion pattern i.e. i) the hypereosinophilia by the hyperproduction of IL-5 and ii) the hyperimmunoglobulinemia E, for which the presence of IL-4 is a "conditio sine qua non".(ABSTRACT TRUNCATED AT 250 WORDS)