Genetics of allergy and allergic sensitization: common variants, rare mutations
Open accessAbstract
Our understanding of the specific genetic lesions in allergy has improved in recent years due to identification of common risk variants from genome-wide association studies (GWAS) and studies of rare, monogenic diseases. Large-scale GWAS have identified novel susceptibility loci and provided information about shared genetics between allergy, related phenotypes and autoimmunity. Studies of monogenic diseases have elucidated critical cellular pathways and protein functions responsible for allergy. These complementary approaches imply genetic mechanisms involved in Th2 immunity, T-cell differentiation, TGFβ signaling, regulatory T-cell function and skin/mucosal function as well as yet unknown mechanisms associated with newly identified genes. Future studies, in combination with data on gene expression and epigenetics, are expected to increase our understanding of the pathogenesis of allergy.
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A significant overlap between susceptibility loci for allergy and autoimmune diseases has been observed.
“In addition to shared genetic effects between different allergy-related diseases, a significant overlap between susceptibility loci for allergy and autoimmune diseases has been observed.495”
From International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis (2018) · cites this paper as [495]
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- [14]BouzigninStockis J Colau D Coulie PG Lucas S Membrane protein GARP is a receptor for latent TGF-beta on the surface of activated human Treg. Eur J Immunol 2009 39 3315 3322 19750484
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- Authors
- Bønnelykke, K., Sparks, R., Waage, J., & Milner, J. D.
- Affiliations
- University of Copenhagen (DK)
- National Institutes of Health (US)
- Corresponding author
- Bønnelykke, Klaus
- Venue
- Current Opinion in Immunology
- Publisher
- Elsevier BV
- Published
- 2015-10
- Volume
- 36
- Pages
- 115-126
- ISSN
- 0952-7915 (ISSN-L)
- PMC
- PMC4610744
- OpenAlex
- W1651524339
- Cited by
- 73
- References
- 77
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 6 · 2023: 4 · 2022: 7 · 2021: 4 · 2020: 8 · 2019: 8 · 2018: 9 · 2017: 8 · 2016: 10 · 2015: 1
- FWCI
- 1.27
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Intramural Research Program of the NIH
- National Institute of Allergy and Infectious Diseases
- Topics
- Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- allergy genetics, allergen sensitization, common genetic variants, rare mutations, genome-wide association study, Th2 immune response, T cell differentiation, TGF-beta signaling, regulatory T cells, autoimmunity, epigenetics
- MeSH terms
- Animals, Humans, Hypersensitivity, Immunization, Mutation, Phenotype, Genetic Variation, Autoimmunity, Quantitative Trait, Heritable, Genetic Predisposition to Disease, Quantitative Trait Loci, Genome-Wide Association Study, Genetic Association Studies
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.
What counts as a claim ›How we measure confidence ›How we check this ›
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