Total IgE levels are considered a useful endophenotype for studying the genetics of atopic diseases. However, the role and significance of genetic factors influencing IgE regulation for atopic diseases as endpoints is unclear.
Recently, genome-wide association studies (GWASs) have been applied to atopic traits with considerable success. A total of seven published GWASs on asthma, one GWAS on eczema, and one GWAS on total IgE have reported 11 new loci. Most of these loci appear to be trait-specific. A notable exception is the Th2 cytokine cluster, where genetic variation seems to be relevant across atopic phenotypes.
GWASs have identified several novel asthma and eczema loci as well as novel loci for IgE levels. In this review, we evaluate the interrelation between these loci and summarize to which degree recent findings on IgE reflect genetic vulnerability for atopic disease.
aDepartment of Dermatology and Allergy, Technische Universität München
bZAUM, Center for Environment and Health, Technische Universität and Helmholtz Zentrum München
cDepartment of Dermatology, Allergy, and Venerology, University Hospital Schleswig-Holstein, Campus Kiel
dGraduate School of Information Science in Health
eInstitute for Medical Statistics and Epidemiology IMSE, Technische Universität München
fDepartment of Dermatology and Allergy, University of Bonn, Bonn, Germany
Correspondence to Stephan Weidinger, MD, Department of Dermatology and Allergy, Technical University Munich, Biedersteiner Str. 28, D-80802 Munich, Germany Tel: +49 89 4140 3396; fax: +49 89 4140 3578; e-mail: email@example.com