TY  - STD
AU  - Ferreira, M. A.
AU  - Vonk, J. M.
AU  - Baurecht, H.
AU  - Marenholz, I.
AU  - Tian, C.
AU  - Hoffman, J. D.
AU  - Helmer, Q.
AU  - Tillander, A.
AU  - Ullemar, V.
AU  - van Dongen, J.
AU  - Lu, Y.
AU  - Ruschendorf, F.
AU  - Esparza-Gordillo, J.
AU  - Medway, C. W.
AU  - Mountjoy, E.
AU  - Burrows, K.
AU  - Hummel, O.
AU  - Grosche, S.
AU  - Brumpton, B. M.
AU  - Witte, J. S.
AU  - Hottenga, J-J
AU  - Willemsen, G.
AU  - Zheng, J.
AU  - Rodriguez, E.
AU  - Hotze, M.
AU  - Franke, A.
AU  - Revez, J. A.
AU  - Beesley, J.
AU  - Matheson, M. C.
AU  - Dharmage, S. C.
AU  - Bain, L. M.
AU  - Fritsche, L. G.
AU  - Gabrielsen, M. E.
AU  - Balliu, B.
AU  - Nielsen, J. B.
AU  - Zhou, W.
AU  - Hveem, K.
AU  - Langhammer, A.
AU  - Holmen, O. L.
AU  - Loset, M.
AU  - Abecasis, G. R.
AU  - Willer, C. J.
AU  - Arnold, A.
AU  - Homuth, G.
AU  - Schmidt, C. O.
AU  - Thompson, P. J.
AU  - Martin, N. G.
AU  - Duffy, D. L.
AU  - Novak, N.
AU  - Schulz, H.
AU  - Karrasch, S.
AU  - Gieger, C.
AU  - Strauch, K.
AU  - Melles, R. B.
AU  - Hinds, D. A.
AU  - Hubner, N.
AU  - Weidinger, S.
AU  - Magnusson, P. K. E.
AU  - Jansen, R.
AU  - Jorgenson, E.
AU  - Lee, Y-A
AU  - Boomsma, D. I.
AU  - Almqvist, C.
AU  - Karlsson, R.
AU  - Koppelman, G. H.
AU  - Paternoster, L.
AU  - LifeLines Cohort Study
PY  - 2017
DA  - 2017//
TI  - Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology
KW  - Asthma/*genetics
KW  - Eczema/*genetics
KW  - Genetic Predisposition to Disease/*genetics
KW  - Genome-Wide Association Study/methods
KW  - Humans
KW  - Hypersensitivity/*genetics
KW  - Phenotype
KW  - Polymorphism
KW  - Single Nucleotide
KW  - Rhinitis
KW  - Allergic
KW  - Seasonal/*genetics
KW  - Risk Factors
AB  - Asthma, hay fever (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals, partly because of a shared genetic origin. To identify shared risk variants, we performed a genome-wide association study (GWAS; n = 360,838) of a broad allergic disease phenotype that considers the presence of any one of these three diseases. We identified 136 independent risk variants (P < 3 x 10(-8)), including 73 not previously reported, which implicate 132 nearby genes in allergic disease pathophysiology. Disease-specific effects were detected for only six variants, confirming that most represent shared risk factors. Tissue-specific heritability and biological process enrichment analyses suggest that shared risk variants influence lymphocyte-mediated immunity. Six target genes provide an opportunity for drug repositioning, while for 36 genes CpG methylation was found to influence transcription independently of genetic effects. Asthma, hay fever and eczema partly coexist because they share many genetic risk variants that dysregulate the expression of immune-related genes.
SN  - 1061-4036
UR  - http://www.ncbi.nlm.nih.gov/pubmed/29083406
UR  - https://doi.org/10.1038/ng.3985
DO  - 10.1038/ng.3985
LA  - English
N1  - PMID:29083406
ID  - Ferreira_etal2017
ER  -