Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology
This large-scale genome-wide association analysis of subjects with asthma, hay fever or eczema provides insights into the shared genetic basis of these allergic diseases. The findings suggest that these diseases partly co-occur because they share many genetic risk variants that dysregulate the expre...
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| Published in | Nature genetics Vol. 49; no. 12; pp. 1752 - 1757 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.12.2017
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | This large-scale genome-wide association analysis of subjects with asthma, hay fever or eczema provides insights into the shared genetic basis of these allergic diseases. The findings suggest that these diseases partly co-occur because they share many genetic risk variants that dysregulate the expression of immune-related genes.
Asthma, hay fever (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals
1
, partly because of a shared genetic origin
2
,
3
,
4
. 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 × 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. |
|---|---|
| AbstractList | Asthma, hay fever (or allergic rhinitis) and eczema (or atopic
dermatitis) often coexist in the same individuals
1
, partly because of a shared genetic origin
2
–
4
. 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
<3x10
-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. 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 × 10 ), 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. Asthma, hay fever (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals1, partly Because of a shared genetic origin2-4. 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. Diseasespecific 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. This large-scale genome-wide association analysis of subjects with asthma, hay fever or eczema provides insights into the shared genetic basis of these allergic diseases. The findings suggest that these diseases partly co-occur because they share many genetic risk variants that dysregulate the expression of immune-related genes. Asthma, hay fever (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals 1 , partly because of a shared genetic origin 2 , 3 , 4 . 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 × 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. |
| Audience | Academic |
| Author | Boomsma, Dorret I Paternoster, Lavinia Zheng, Jie Brumpton, Ben M Revez, Joana A Beesley, Jonathan Nielsen, Jonas B van Dongen, Jenny Balliu, Brunilda Tian, Chao Rodríguez, Elke Duffy, David L Dharmage, Shyamali C Holmen, Oddgeir L Novak, Natalija Hübner, Norbert Hveem, Kristian Arnold, Andreas Homuth, Georg Witte, John S Ullemar, Vilhelmina Ferreira, Manuel A Hottenga, Jouke-Jan Willemsen, Gonneke Franke, Andre Jansen, Rick Almqvist, Catarina Medway, Chris W Langhammer, Arnulf Gabrielsen, Maiken E Fritsche, Lars G Matheson, Melanie C Baurecht, Hansjörg Helmer, Quinta Rüschendorf, Franz Karrasch, Stefan Tillander, Annika Melles, Ronald B Burrows, Kimberley Hoffman, Joshua D Vonk, Judith M Hinds, David A Schulz, Holger Schmidt, Carsten O Thompson, Philip J Grosche, Sarah Koppelman, Gerard H Willer, Cristen J Gieger, Christian Weidinger, Stephan Magnusson, Patrik K E Martin, Nicholas G Karlsson, Robert Mountjoy, Edward Zhou, Wei Marenholz, Ingo Esparza-Gordillo, Jorge Hummel, Oliver Jorgenson, Eric Bain, Lisa M Hotze, Melanie Lu, Yi Løset, Mari Stra |
| AuthorAffiliation | 20 Department of Internal Medicine, University of Michigan, Ann Arbor, USA 6 Research, 23andMe, Mountain View, California, USA 13 Department of Thoracic Medicine, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway 24 Clinic and Polyclinic of Dermatology, University Medicine Greifswald, Greifswald, Germany 31 Institute and Outpatient Clinic for Occupational, Social and Environmental Medicine, Ludwig-Maximilians-Universität, Munich, Germany 2 Epidemiology, University of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands 23 Center for Statistical Genetics, University of Michigan, Ann Arbor, USA 33 Institute of Genetic Epidemiology, Helmholtz Zentrum Munchen - German Research Center for Environmental Health , Neuherberg, Germany 5 Clinic for Pediatric Allergy, Experimental and Clinical Research Center of Charité Universitätsmedizin Berlin and Max Delbrück Center, Berlin, Germany 15 Institute of Clinical Mole |
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organization: MRC Integrative Epidemiology Unit, School of Social and Community Medicine, University of Bristol |
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| Issue | 12 |
| Language | English |
| License | Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms |
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| Notes | A full list of members and affiliations appears in the Supplementary Note These authors jointly supervised this work. Current address: GlaxoSmithKline, Stevenage, UK |
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| Snippet | This large-scale genome-wide association analysis of subjects with asthma, hay fever or eczema provides insights into the shared genetic basis of these... 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... Asthma, hay fever (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals1, partly Because of a shared genetic... Asthma, hay fever (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals 1 , partly because of a shared genetic origin... |
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| SubjectTerms | 38/39 45/43 631/208/205/2138 692/699/249/2510/1415 692/699/249/2510/31 692/699/249/2510/9 Age Agriculture Allergic rhinitis Allergies Animal Genetics and Genomics Asthma Asthma - genetics Atopic dermatitis Biological activity Biomedicine Cancer Research CpG islands Dermatitis Disease DNA methylation Eczema Eczema - genetics Gene expression Gene Function Genes Genetic aspects Genetic effects Genetic Predisposition to Disease - genetics Genetic variation Genome-wide association studies Genome-Wide Association Study - methods Genomes Hay Hay fever Health aspects Heritability Human Genetics Humans Hypersensitivity - genetics Immunity letter Lymphocytes Medicin och hälsovetenskap Methods Phenotype Polymorphism, Single Nucleotide Rhinitis Rhinitis, Allergic, Seasonal - genetics Risk analysis Risk Factors Risk sharing Skin diseases Studies Transcription |
| Title | Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology |
| URI | https://link.springer.com/article/10.1038/ng.3985 https://www.ncbi.nlm.nih.gov/pubmed/29083406 https://www.proquest.com/docview/1972249419 https://pubmed.ncbi.nlm.nih.gov/PMC5989923 http://kipublications.ki.se/Default.aspx?queryparsed=id:137129768 |
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