[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 necessary 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 numbers.
Böhm
I
I
Universitäts-Hautklinik, Rheinischen Friedrich-Wilhelms-Universität Bonn.
Bauer
R
R
D000485:Allergens / Q000276:immunology; D016207:Cytokines / Q000502:physiology; D003876:Dermatitis, Atopic / Q000235:genetics / Q000276:immunology*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007801:Langerhans Cells / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
D000485:Allergens; D016207:Cytokines; D007073:Immunoglobulin E