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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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“For example, the HLA-DQB1, TLR1, WDR36, LRRC32, IL1RL1, GSDMA, TSLP, IL33, SMAD3 genes involved in the pathogenesis of certain allergic diseases are critical for the development of phenotype according to the “atopic march” scenario (Ferreira et al., 2014).”
BackgroundLiang, S., Long, J., Long, J., Wei, X., Yang, M., Yang, M., Qin, H.-J., Zhou, J., & Hai-li, L. (2020) · Combinatorial Chemistry & High Throughput Screening · doi:10.2174/1386207326666230602161939 · Cited by 2
Ma, Y., Xu, H., Li, Y., Kim, H., Xu, L.-L., Miao, L., Xu, P., Mao, F., Zhou, S., Zhou, W., et al. (2025) · Genome biology · doi:10.1186/s13059-025-03827-9 · Cited by 2
“Ferreira et al. identified this SNP as a risk variant associated with the asthma with hay fever phenotype [37].”
Molecular and genomic basis of bronchial asthma
Gupta, A., Chakraborty, S., & Agrawal, A. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-809356-6.00020-4 · Cited by 2
CLEC16A variants conferred a decreased risk to allergic rhinitis in the Chinese population
Niu, Y., Wang, H., Li, Z., Shamsi, B. H., Liu, M., Liu, J., Wang, Q., & Liu, Y. (2022) · Frontiers in Genetics · doi:10.3389/fgene.2022.1053761 · Cited by 2
“, they observed CLEC16A rs62026376 associated with increased asthma with hay fever risk (Ferreira et al., 2014).”
BackgroundHenderson, A. J. (2019) · Elsevier eBooks · doi:10.1016/b978-0-323-44887-1.00042-0 · Cited by 2
Self-citationІмуногенетичні предиктори алергічного риніту
Турова, Л. О., Naumenko, O. M., & Bobyr, V. V. (2023) · Asthma and allergy · doi:10.31655/2307-3373-2023-3-49-57 · Cited by 1
Venkateswaran, V. R., She, R., Gui, H., Luzum, J. A., Bryson, T. D., Malouf, Z. E., Williams, L. K., Sabbah, H. N., Gardell, S. J., & Lanfear, D. E. (2024) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2024.1409340 · Cited by 1
Xuan, L., Ren, L., Zhang, W., & An, Z. (2025) · Journal of Inflammation Research · doi:10.2147/jir.s527640 · Cited by 1
“nucleotide polymorphism was also related to the risk of asthma with hay fever 52 and COPD.”
Belitardo, E. M. M. D. A., Marques, C. R., da Silva, T. M., da Silva, E. S., Aguiar, E. R. G. R., Barreto, M. L., Alcântara‐Neves, N. M., & Figueiredo, C. A. (2025) · Cytokine · doi:10.1016/j.cyto.2025.157073 · Cited by 1
Nagino, K., Inomata, T., Ebihara, N., Midorikawa‐Inomata, A., Fujio, K., Kobayashi, H., & Nakao, S. (2025) · Allergology International · doi:10.1016/j.alit.2025.11.008 · Cited by 1
Risk factors and protective factors in pediatric patients with allergic rhinitis
Chun, Y. H., Kim, M., Kim, H., Rha, Y.-H., Park, Y., Park, Y. M., Sung, M., Shin, Y. H., Yum, H. Y., Lee, K. S., et al. (2022) · Allergy Asthma & Respiratory Disease · doi:10.4168/aard.2022.10.2.73 · Cited by 1
Basic genetics and epigenetics for the immunologist and allergist
Chen, M., Lejeune, S., Zhou, X., & Nadeau, K. C. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-95061-9.00005-9 · Cited by 1
Li, H., Yu, Z., Du, F., Song, L., Gao, Y., & Shi, F. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1323072 · Cited by 1
The Development of Allergic Rhinitis in Childhood
Wahn, U., Keil, T. O. P., & Grabenhenrich, L. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-420226-9.00007-3 · Cited by 2
Genetics and Epigenetic Regulation in Allergic Diseases
Kuo, C., & Hung, C. (2015) · Translational bioinformatics · doi:10.1007/978-94-017-7444-4_4 · Cited by 1
“Similar to ORMDL3, IL-33 has been reported in several other GWASs of asthma (Bonnelykke et al. 2014b; Ferreira et al. 2014; Torgerson et al. 2011a).”
ResultMcGeachie, M. J., Croteau‐Chonka, D. C., & Weiss, S. T. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-800685-6.00013-8 · Cited by 1
Genetics of "atopic march" syntropy
Bragina, E. Y., Freidin, M. B., & Puzyrev, V. P. (2020) · Сибирский научный медицинский журнал · doi:10.15372/ssmj20200501 · Cited by 1
“2), из них 9 SNP расположены в известных локусах риска аллергических заболеваний или рядом с ними: HLA-DQB1 (р = 4 × 10–14), TLR1 (р = 5 × 10-12), WDR36 (р = 3 × 10–11), LRRC32 (р = 5 × 10–11), IL1RL1 (р = 4 × 10–11), GSDMA (р = 4 × 10–10), TSLP (р = 10–9), IL33 (р = 2 × 10–9) и SMAD3 (р = 4 × 10–9) [25].”
Evaluating metagenomic quantifications from next-generation sequencing data
Laver, T. W. (2014) · Open Research Exeter (University of Exeter) · Cited by 1
Leveraging auxiliary data from arbitrary distributions to boost GWAS discovery with Flexible cFDRPreprint
Hutchinson, A., Reales, G., Willis, T. W., & Wallace, C. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.12.04.411710 · Cited by 1
Genetics of Asthma: Insights From Genome Wide Association Studies
Cooper, R. M., Bingham, K., Portelli, M. A., & Sayers, I. (2021) · Elsevier eBooks · doi:10.1016/b978-0-08-102723-3.00155-4 · Cited by 1
ITA chez l’enfant, prévention de l’asthme et de nouvelles sensibilisations ?
Payot, F. (2016) · Revue française d'allergologie · doi:10.1016/j.reval.2016.02.010
Functional analysis of polymorphisms in asthma genes : TSLP and IL1RL1
Akhabir, L. (2014) · cIRcle (University of British Columbia) · doi:10.14288/1.0166983
Miller, D. E., Forney, C., Rochman, M., Cranert, S., Habel, J., Rymer, J., Lynch, A., Schroeder, C., Lee, J., Sauder, A., et al. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/359638
Mogushi, K., Murakawa, Y., & Kawaji, H. (2018) · Respiratory disease series · doi:10.1007/978-981-10-8144-6_17
The multifactorial nature of food allergy
van Ginkel, C. D. (2018) · University of Groningen research database (University of Groningen / Centre for Information Technology)
Qualitative signs of digital dermatoglyphics as markers of diseases of atopic nature
Черкасов, В. Г., Maievskyi, O., Serheta, I. V., Makarchuk, I. M., & Smolko, N. M. (2019) · Biomedical and Biosocial Anthropology · doi:10.31393/bba34-2019-01
“It is noted that individuals of different sex, age and type of body structure are very strikingly affected by these diseases [6, 23, 25, 26, 28, 29].”
BackgroundHirahara, K., & Nakayama, T. (2018) · PubMed · doi:10.15036/arerugi.67.179
Epigenetics of allergies: From birth to childhood
DeVries, A., & Vercelli, D. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-817964-2.00012-5
Epigenetic Trajectories to Childhood Asthma
DeVries, A. (2018) · UA Campus Repository (The University of Arizona)
A powerful replicability analysis of genome-wide association studiesPreprint
Li, Y., Lei, H., Wen, X., & Cao, H. (2023) · medRxiv · doi:10.1101/2023.09.04.23295018
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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