Three new risk genes for atopic dermatitis identified

Kiel, Germany 3 Januar 2012  WIth an estimated incidence of about 20 percent in children and approximately five percent in adults, atopic dermatitis is one of the most common chronic skin diseases in western industrialized nations. It often precedes the development of hay fever and asthma and is associated with a number of other diseases. A large portion of the risk of developing atopic dermatitis and allergies is inherited. In combination with environmental influences, it leads to the development of disease.

Largest ever international genetic study of atopic dermatitis

Under the direction of Professor Stephan Weidinger, Cluster of Excellence “Inflammation at Interfaces” (Department of Dermatology UKSH, Kiel Campus, and Faculty of Medicine, CAU), and Dr. David Evans of the University of Bristol and Dr. Joachim Heinrich of the Helmoholtz Zentrum München (German Research Center for Environmental Health, Munich) within the framework of the “EAGLE” Consortium (EArly Genetics and Lifecourse Epidemiology), the world’s largest genetic study to date focused on  atopic dermatitis has been conducted. Researchers from twelve countries, including Australia, Canada, the USA and nine European countries, have, in co-operation and within two years, studied the entire genome of more than 10,000 patients and 40,000 healthy individuals.

The study showed three gene variants, previously not associated with atopic dermatitis, brought marked effects on the risk of disease. Two of theses gene variants play a role in maintaining the skin’s natural barrier, while the third gene variant has an effect on immune regulation and has already been linked with asthma and allergic diseases. Professor Stephan Weidinger commented: “Our findings show that there are more genes with different functions involved in the formation of atopic dermatitis than previously thought. They help us to better understand the causes of the disease and can contribute to the development of new tests for risk assessment and new treatment methods. Up to now, we knew of two well-studied risk genes, which we were able to newly confirm. We can now add the three new risk genes, which we have identified. We turn now to the question of how, with this newly acquired knowledge, we can improve prevention and clinical diagnostics in order to develop new therapeutic approaches.”

The findings of the study are currently available on the website of the journal Nature Genetics. Link to the abstract “Meta-analysis of genome-wide association studies on atopic dermatitis identifies three novel risk loci” on the website of Nature Genetics: http://www.nature.com/ng/journal/vaop/ncurrent/full/ng.1017.html

The Cluster of Excellence "Inflammation at Interfaces"

The Inflammation Research Excellence Cluster follows a unique, interdisciplinary research approach in order to decode the causes of chonic inflammation and to develop therapies for healing. The research association brings together the competences of approximately 200 geneticists, biologists, nutritionists and physicians from Kiel University and the University of Lübeck, the Research Institute Borstel and the Max Planck Institute for Evolutionary Biology, Plön. In Germany alone, millions of people suffer from chronic inflammation of the lungs (asthma), the skin (psoriasis), the intestines (Crohn’s disease) and the brain (Parkinson’s disease). The trigger is a disorder of the immune system: it incessantly activates inflammatory mediators and defense cells, thereby destroying healthy tissue. The number of sufferers increases daily. This phenomenon of modern civilization has become the challenge for 21st Century medicine. Accordingly, in 2007 the German Federal Government and the German Research Foundation declared the decoding of the complex inflammation mechanism to be a national scientific priority.

Business Office of the Inflammation Research Excellence Cluster:

Dr. Helga Andree, Office Manager, T: +49.431.880-5536, E: info@inflammation-at-interfaces.de

Press contact: Susanne Weller, M: +49.172.308 41 36, E: s.weller@weller-media.com