[Th1 cells, Th2 cells and atopic dermatitis] NLM AIDSLINE Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.

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[Th1 cells, Th2 cells and atopic dermatitis]

Hautarzt. 1997 Apr;48(4):223-7. Unique Identifier : AIDSLINE MED/97295467
Bohm I; Bauer R; Universitats-Hautklinik, Rheinischen Friedrich-Wilhelms-Universitat; Bonn.


Abstract: 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.
Keywords: *Dermatitis, Atopic/IMMUNOLOGY *Th1 Cells/IMMUNOLOGY *Th2 Cells/IMMUNOLOGYKWDdermatitis,atopic/immunologyKWDth1cells/immunologyKWDth2cells/immunology
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Copyright © 1997 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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