Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology
Open accessAbstract
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 × 10−8), 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.
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The main epigenetic studies in AD are related to the DNA methylation of two genes, NLRP2 (involved in macrophage activity) and PITPNM2 (related to neutrophils), both associated with smoking.
“The main epigenetic studies in AD are related to the DNA methylation of two genes, NLRP2 (involved in macrophage activity) and PITPNM2 (related to neutrophils), both associated with smoking.”
From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [41]
The Abstract (page unavailable) reports a significant association between smoking and PITPNM2 methylation and describes PITPNM2 as potentially involved in neutrophil function. It says this was the only significant smoking–methylation association found; our copy does not support the claimed smoking association for NLRP2 or its proposed macrophage role, nor does it characterize these two genes as the focus of the main epigenetic studies in AD. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThe association of eczema herpeticum and serum IgE levels with methylation in the IL-4 and IL-13 genes has been found.
“Also, the association of eczema herpeticum and serum IgE levels with methylation in the IL-4 and IL-13 genes.”
From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [41]
The methylation analysis and Online Methods describe associations between CpG methylation and gene expression, then tests of five allergic-disease risk factors. Searches for eczema herpeticum, serum IgE, and IL-4/IL-13 methylation found no passage in our copy linking either outcome to methylation in those genes. The reported smoking–PITPNM2 association does not address the cited claim. (LLM, conf=0.76)
Experimental — accuracy not yet measuredA GWAS of allergic diseases points to a credible missense risk variant in FAM105A.
“Although little is known about FAM105A function, GWAS of allergic diseases implicates a credible missense risk variant in this gene (Ferreira et al., 2017).”
From Genome-wide CRISPR Screens in Primary Human T Cells Reveal Key Regulators of Immune Function (2018) · cites this paper as Ferreira et al., 2017
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Immune disease risk variants regulate gene expression dynamics during CD4+ T cell activation
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Self-citationAn atlas of gene regulatory elements in adult mouse cerebrum
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Comorbidities of atopic dermatitis—what does the evidence say?
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Single-cell DNA methylation and 3D genome architecture in the human brain
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Resource profile and user guide of the Polygenic Index Repository
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Self-citationThe genetics of asthma and the promise of genomics-guided drug target discovery
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Self-citationPrioritization of candidate causal genes for asthma in susceptibility loci derived from UK Biobank
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Advances and novel developments in allergic rhinitis
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Chromatin activity at GWAS loci identifies T cell states driving complex immune diseases
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Self-citationCardiometabolic Traits, Sepsis, and Severe COVID-19
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Self-citationHuman germline heterozygous gain-of-function <i>STAT6</i> variants cause severe allergic disease
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Mechanisms by Which Atopic Dermatitis Predisposes to Food Allergy and the Atopic March
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Adult‐onset eosinophilic airway diseases
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IL-4/IL-13 axis as therapeutic targets in allergic rhinitis and asthma
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Self-citationAdvances in asthma and allergic disease genetics: Is bigger always better?
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Self-citationAllergy and atopy from infancy to adulthood
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Recent developments and advances in atopic dermatitis and food allergy
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The Genetics and Genomics of Asthma
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Self-citationA genome-wide association meta-analysis identifies new eosinophilic esophagitis loci
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Chronic calcium signaling in IgE+ B cells limits plasma cell differentiation and survival
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Eleven loci with new reproducible genetic associations with allergic disease risk
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Genetic determinants of paediatric food allergy: A systematic review
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Update on the pathogenesis of atopic dermatitis.
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Germline Features Associated with Immune Infiltration in Solid Tumors
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Genetic Susceptibility Loci in Genomewide Association Study of Cluster Headache
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The familial aggregation of atopic diseases and depression or anxiety in children
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Self-citationGenetic and Epigenetic Fine Mapping of Complex Trait Associated Loci in the Human Liver
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Integrative Omics Approach to Identifying Genes Associated With Atrial Fibrillation
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Immune disease variants modulate gene expression in regulatory CD4+ T cells
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One march, many paths: Insights into allergic march trajectories
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Atopic phenotypes and their implication in the atopic march
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- Authors
- 23andMe Research Team, Ferreira, M. A., collaborators, A., BIOS consortium, Study, L. C., Vonk, J. M., Baurecht, H., Marenholz, I., Tian, C., Hoffman, J. D., Helmer, Q., Tillander, A., Ullemar, V., van Dongen, J., Lu, Y., Rüschendorf, F., Esparza-Gordillo, J., Medway, C. W., Mountjoy, E., Burrows, K., Hummel, O., Grosche, S., Brumpton, B. M., Witte, J. S., Hottenga, J.-J., Willemsen, G., Zheng, J., Rodríguez, E., Hotze, M., Franke, A., Revez, J. A., Beesley, J., Matheson, M. C., Dharmage, S. C., Bain, L. M., Fritsche, L. G., Gabrielsen, M. E., Balliu, B., Nielsen, J. B., Zhou, W., Hveem, K., Langhammer, A., Holmen, O. L., Løset, M., Abecasis, G. R., Willer, C. J., Arnold, A., Homuth, G., Schmidt, C. O., Thompson, P. J., Martin, N. G., Duffy, D. L., Novak, N., Schulz, H., Karrasch, S., Gieger, C., Strauch, K., Melles, R. B., Hinds, D. A., Hübner, N., Weidinger, S., Magnusson, P. K. E., Jansen, R., Jorgenson, E., Lee, Y.-A., Boomsma, D. I., Almqvist, C., Karlsson, R., Koppelman, G. H., & Paternoster, L.
- Affiliations
- QIMR Berghofer Medical Research Institute (AU)
- University Medical Center Groningen (NL)
- University Hospital Schleswig-Holstein (DE)
- 23andMe (United States) (US)
- University of California, San Francisco (US)
- Karolinska Institutet (SE)
- Max Delbrück Center (DE)
- University of Bristol (GB)
- Norwegian University of Science and Technology (NO)
- Christian-Albrechts-Universität zu Kiel (DE)
- The University of Melbourne (AU)
- University of Michigan (US)
- Universitätsmedizin Greifswald (DE)
- The University of Western Australia (AU)
- University Hospital Bonn (DE)
- Helmholtz Munich (DE)
- Kaiser Permanente (US)
- Karolinska University Hospital (SE)
- Corresponding author
- Ferreira, Manuel A
- ORCID
- Ferreira, Manuel A
- Vonk, Judith M
- Baurecht, Hansjörg
- Marenholz, Ingo
- Tian, Chao
- Hoffman, Joshua D
- Tillander, Annika
- Ullemar, Vilhelmina
- Lu, Yi
- Rüschendorf, Franz
- Mountjoy, Edward
- Burrows, Kimberley
- Hummel, Oliver
- Grosche, Sarah
- Brumpton, Ben M
- Witte, John S
- Hottenga, Jouke-Jan
- Willemsen, Gonneke
- Zheng, Jie
- Rodríguez, Elke
- Franke, Andre
- Revez, Joana A
- Matheson, Melanie C
- Dharmage, Shyamali C
- Fritsche, Lars G
- Gabrielsen, Maiken E
- Balliu, Brunilda
- Nielsen, Jonas B
- Zhou, Wei
- Hveem, Kristian
- Langhammer, Arnulf
- Løset, Mari
- Abecasis, Gonçalo R
- Willer, Cristen J
- Arnold, Andreas
- Homuth, Georg
- Schmidt, Carsten O
- Thompson, Philip J
- Martin, Nicholas G
- Duffy, David L
- Novak, Natalija
- Schulz, Holger
- Karrasch, Stefan
- Gieger, Christian
- Strauch, Konstantin
- Melles, Ronald B
- Hinds, David A
- Hübner, Norbert
- Weidinger, Stephan
- Magnusson, Patrik K E
- Jansen, Rick
- Jorgenson, Eric
- Lee, Young-Ae
- Boomsma, Dorret I
- Almqvist, Catarina
- Karlsson, Robert
- Koppelman, Gerard H
- Paternoster, Lavinia
- Venue
- Nature Genetics
- Published
- 2017-10-30
- Volume
- 49
- Issue
- 12
- Pages
- 1752-1757
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC5989923
- OpenAlex
- W2765256236
- Semantic Scholar
- 08c8383033e73b5aa7bee3306e4e91cbd16ae672
- Cited by
- 550
- References
- 51
- Citations by year
- 2026: 44 · 2025: 45 · 2024: 61 · 2023: 62 · 2022: 77 · 2021: 74 · 2020: 78 · 2019: 70 · 2018: 35 · 2017: 3
- FWCI
- 37.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion, other-oa)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion, other-oa)
- Explore Bristol Research (publishedVersion, other-oa)
- VU Research Portal (publishedVersion, other-oa)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Bristol Research (University of Bristol) (submittedVersion, other-oa)
- UWA Profiles and Research Repository (UWA) (submittedVersion, other-oa)
- MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Minerva Access (University of Melbourne) (submittedVersion)
- Site cant be reached (submittedVersion, other-oa)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Norges Teknisk-Naturvitenskapelige Universitet
- Wellcome Trust (102215)
- QIMR Berghofer Medical Research Institute
- University of Bristol
- Rijksuniversiteit Groningen
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek (480-15-001)
- Lundbeckfonden (R220-2016-1434)
- Karolinska Institutet
- Universitair Medisch Centrum Groningen
- St. Olavs Hospital Universitetssykehuset i Trondheim
- Medical Research Council (MR/J012165/1, MC_PC_12028)
- National Cancer Institute (R25CA112355)
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Keywords
- asthma, allergic rhinitis, atopic dermatitis, allergic diseases, genetic susceptibility loci, immune gene expression, lymphocyte-mediated immunity, drug repurposing, CpG methylation, transcriptional regulation
- MeSH terms
- Asthma, Eczema, Rhinitis, Allergic, Seasonal, Humans, Hypersensitivity, Phenotype, Risk Factors, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Genome-Wide Association Study
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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