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Genome-wide association analysis identifies 11 risk variants associated with the asthma with hay fever phenotype
Open accessAbstract
Background To date, no genome-wide association study (GWAS) has considered the combined phenotype of asthma with hay fever. Previous analyses of family data from the Tasmanian Longitudinal Health Study provide evidence that this phenotype has a stronger genetic cause than asthma without hay fever.Objective We sought to perform a GWAS of asthma with hay fever to identify variants associated with having both diseases.Methods We performed a meta-analysis of GWASs comparing persons with both physician-diagnosed asthma and hay fever (n = 6,685) with persons with neither disease (n = 14,091).Results At genome-wide significance, we identified 11 independent variants associated with the risk of having asthma with hay fever, including 2 associations reaching this level of significance with allergic disease for the first time: ZBTB10 (rs7009110; odds ratio [OR], 1.14; P = 4 × 10(-9)) and CLEC16A (rs62026376; OR, 1.17; P = 1 × 10(-8)). The rs62026376:C allele associated with increased asthma with hay fever risk has been found to be associated also with decreased expression of the nearby DEXI gene in monocytes. The 11 variants were associated with the risk of asthma and hay fever separately, but the estimated associations with the individual phenotypes were weaker than with the combined asthma with hay fever phenotype. A variant near LRRC32 was a stronger risk factor for hay fever than for asthma, whereas the reverse was observed for variants in/near GSDMA and TSLP. Single nucleotide polymorphisms with suggestive evidence for association with asthma with hay fever risk included rs41295115 near IL2RA (OR, 1.28; P = 5 × 10(-7)) and rs76043829 in TNS1 (OR, 1.23; P = 2 × 10(-6)).Conclusion By focusing on the combined phenotype of asthma with hay fever, variants associated with the risk of allergic disease can be identified with greater efficiency.
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“SNPs in different TLRs have been associated with AR in both GWASs (TLR1, TLR6, TLR10)486,487 and candidate gene studies (TLR8), as discussed in the next paragraph.494”
From International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis (2018) · cites this paper as [486]
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“SNPs in leucine-rich repeat-containing protein 32 (LRRC32) have been strongly associated with AR in 3 of the GWASs,486-488 and with asthma,487,489 eczema,488,490 and other allergy-related comorbidities.486,489,491”
From International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis (2018) · cites this paper as [486]
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“DEXI is expressed in the lung, as well as in relevant immune cell types, such as CD4(1) T cells and B cells.(54) However, its function is unknown, and therefore studying its role in the immune system might provide new insights into the cause of allergic disease.”
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“We found that considering asthma and hay fever as 3 mutually exclusive phenotypes was informative; the strengths and the familial aspects of their relationship with eczema in infancy differed across the 3 outcomes.(24) Specifically, the childhood disease associations with infantile eczemawere more pronounced and more…”
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6: Rhinitis and asthma: united airway disease
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“The allele associated with an increased risk of asthma with hay fever decreases DEXI expression, which is consistent with recent reports for autoimmune disease– associated variants.(54,55) This suggests that DEXI is a plausible causal gene underlying the observed association with allergic disease.”
ResultMultivariate genetic analysis of atopy phenotypes in a selected sample of twins
Thomsen, S. F., Ulrik, C. S., Kyvik, K. O., Ferreira, M. A. R., & Backer, V. (2006) · Clinical & Experimental Allergy · doi:10.1111/j.1365-2222.2006.02512.x · Cited by 36 · cited 1×
“Consistent with the latter hypothesis, results from twin and family studies have estimated that both diseases share 50% to 90% of their genetic susceptibility and 20% to 50% of their environmental susceptibility.(7,8) Genome-wide association studies (GWASs) are a proved approach to discover genetic variants associated…”
ResultSelf-citationTakahashi, K., Hayashi, N., Shimokawa, T., Umehara, N., Kaminogawa, S., & Ra, C. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m800498200 · Cited by 29
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Self-citationInternational Consensus Statement on Allergy and Rhinology: Allergic Rhinitis
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Self-citation
Metadata
- Authors
- Ferreira, M. A. R., Matheson, M. C., Tang, C. S., Granell, R., Ang, W., Hui, J., Kiefer, A. K., Duffy, D. L., Baltic, S., Danoy, P., Bui, M., Price, L., Sly, P. D., Eriksson, N., Madden, P. A., Abramson, M. J., Holt, P. G., Heath, A. C., Hunter, M., Musk, B., Robertson, C. F., Le Souëf, P., Montgomery, G. W., Henderson, A. J., Tung, J. Y., Dharmage, S. C., Brown, M. A., James, A., Thompson, P. J., Pennell, C., Martin, N. G., Evans, D. M., Hinds, D. A., & Hopper, J. L.
- Affiliations
- QIMR Berghofer Medical Research Institute (AU)
- The University of Melbourne (AU)
- University of Bristol (GB)
- The University of Western Australia (AU)
- 23andMe (United States) (US)
- Translational Research Institute (AU)
- Queensland Children’s Medical Research Institute (AU)
- Washington University in St. Louis (US)
- Monash University (AU)
- The Kids Research Institute Australia (AU)
- Murdoch Children's Research Institute (AU)
- Corresponding author
- Ferreira, Manuel A.R.
- Hopper, John L.
- ORCID
- Ferreira, Manuel A.R.
- Matheson, Melanie C.
- Tang, Clara S.
- Granell, Raquel
- Hui, Jennie
- Duffy, David L.
- Baltic, Svetlana
- Bui, Minh
- Sly, Peter D.
- Eriksson, Nicholas
- Madden, Pamela A.
- Abramson, Michael J.
- Holt, Patrick G.
- Heath, Andrew C.
- Hunter, Michael
- Montgomery, Grant W.
- Henderson, A. John
- Tung, Joyce Y.
- Dharmage, Shyamali C.
- Brown, Matthew A.
- Thompson, Philip J.
- Pennell, Craig
- Martin, Nicholas G.
- Evans, David M.
- Hinds, David A.
- Hopper, John L.
- Venue
- Journal of Allergy and Clinical Immunology
- Publisher
- Elsevier BV
- Published
- 2014-06
- Volume
- 133
- Issue
- 6
- Pages
- 1564-1571
- ISSN
- 0091-6749 (ISSN-L)
- PMC
- PMC4280183
- OpenAlex
- W2081882488
- Cited by
- 216
- References
- 64
- Citations by year
- 2026: 7 · 2025: 12 · 2024: 11 · 2023: 18 · 2022: 17 · 2021: 15 · 2020: 19 · 2019: 16 · 2018: 25 · 2017: 13 · 2016: 25 · 2015: 24 · 2014: 14
- FWCI
- 16.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Allergy and Clinical Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- QUT ePrints (Queensland University of Technology) (submittedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion, cc-by-nc-nd)
- Figshare (submittedVersion, cc-by)
- The HKU Scholars Hub (University of Hong Kong) (submittedVersion)
- Funders
- March of Dimes Foundation
- Mesothelioma Applied Research Foundation
- Pfizer
- Wellcome Trust
- QIMR Berghofer Medical Research Institute
- Cystic Fibrosis in Australia
- Raine Medical Research Foundation (003209)
- Women and Infants Research Foundation
- Australian Cystic Fibrosis Research Trust
- University of Melbourne
- National Institutes of Health (389875, QLG2-CT-2002-01254, AA10248, MH66206, AA11998, AA13321, AA17688, AA13320, DA12854, AA07728)
- Canadian Institutes of Health Research (MOP82893)
- Medical Research Council (MC_PC_15018)
- Australian Research Council (DP0343921)
- National Health and Medical Research Council (A7960034, 496739, 1044829, 572613, A79906588, 003209, 403981, 389927, 389891, 552485, DP0212016, 552498, 442981, 436959, 389938, 241944, 339462, 442915, 389875, 490321, MOP-82893, 613627, 1006215, A79801419, DP0770096, 491246, 389892)
- National Institute on Alcohol Abuse and Alcoholism (AA-10248, AA11998, R37AA007728, K05AA017688, R01AA010249, R01AA013321, P50AA011998, AA13320, AA13321, AA17688, P60AA011998, R01AA007728, R01AA013326, AA13326, R01AA013320, R01AA014041, AA14041, R01AA007535, AA-07728)
- National Heart, Lung, and Blood Institute (R43HL115873)
- National Institute of Mental Health (MH66206, R01MH066206)
- National Institute on Drug Abuse (R56DA012854, R25DA027995, DA12854, R01DA012854)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
- Keywords
- allergic rhinitis, asthma, genetic risk variants, ZBTB10, CLEC16A, LRRC32, GSDMA, thymic stromal lymphopoietin, IL2RA, TNS1, DEXi, monocytes, Tasmanian Longitudinal Health Study
- MeSH terms
- Adult, Alleles, Asthma, Female, Gene Frequency, Rhinitis, Allergic, Seasonal, Humans, Male, Middle Aged, Monosaccharide Transport Proteins, Phenotype, Repressor Proteins, Genetic Variation, Linkage Disequilibrium, Odds Ratio, Polymorphism, Single Nucleotide, Lectins, C-Type, Quantitative Trait Loci, Genome-Wide Association Study, Young Adult
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