Th1-cells, Th2-cells and atopic dermatitis

The immunological hallmark of atopic dermatitis (AD) is a Th1/Th2 dysbalance. The reaction to high molecular weight environmental allergens (e.g. pollen, house dust mites), production of IgE and activation of eosinophil granulocytes result from Th2 dominance. The Th2-cytokine interleukin-4, (IL-4) is necessary for IgE synthesis. Additionally, IL-4 inhibits the generation of Th1-cells. The marker cytokine of Th1-cells, interferon gamma (IFN gamma), exhibits reciprocal effects. It inhibits IgE synthesis and Th2 expansion, but supports Th1-cell growth. Beside the well known mechanisms of IgE-mediated immediate type reactions, the relevance of IgE for the pathogenesis of AD seems to be likely since the discovery of IgE-receptors upon Langerhans cell surfaces. Langerhans cell-bound IgE may be possibly neccessary for the presentation of high molecular weight aero-allergens. Analyses of Th subsets at different intervals after allergen challenge showed, that Th2-cells play an important role in the initial phase of inflammatory reactions whereas in later stages Th1-cells can be detected in greater numbes.