Abstract

Chronic inflammatory disorders such as Crohn disease, atopic eczema, asthma and psoriasis are triggered by hitherto unknown environmental factors that function on the background of some polygenic susceptibility. Recent technological advances have allowed us to unravel the genetic aetiology of these and other complex diseases. Using Crohn disease as an example, we show how the discovery of susceptibility genes furthers our understanding of the underlying disease mechanisms and how it will, ultimately, give rise to new therapeutic developments. The long-term goal of such endeavours is to develop targeted prophylactic strategies. These will probably target the molecular interaction on the mucosal surface between the products of the genome and the microbial metagenome of a patient.

Author affiliations

1. Institute for Clinical Molecular Biology, Center for Conservative Medicine, Christian-Albrechts-University Kiel, Schittenhelmstr. 12, 24105 Kiel, Germany.
2. Department of Computational Biology and Applied Algorithmics, Max-Planck-Institute for Informatics, Stuhlsatzenhausweg 85, 66123 Saarbrücken, Germany.
3. Institute for Medical Informatics and Statistics, Center of Expertise in Genetic Epidemiology (GEM), Christian-Albrechts-University Kiel, Brunswiker Str. 10, 24105 Kiel, Germany.

Correspondence to: Stefan Schreiber¹ Email: s.schreiber@mucosa.de

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