The genetics of asthma and allergic disease: a 21st century perspective
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Summary: Asthma and allergy are common conditions with complex etiologies involving both genetic and environmental contributions. Recent genome‐wide association studies (GWAS) and meta‐analyses of GWAS have begun to shed light on both common and distinct pathways that contribute to asthma and allergic diseases. Associations with variation in genes encoding the epithelial cell‐derived cytokines, interleukin‐33 (IL‐33) and thymic stromal lymphopoietin (TSLP), and the IL1RL1 gene encoding the IL‐33 receptor, ST2, highlight the central roles for innate immune response pathways that promote the activation and differentiation of T‐helper 2 cells in the pathogenesis of both asthma and allergic diseases. In contrast, variation at the 17q21 asthma locus, encoding the ORMDL3 and GSDML genes, is specifically associated with risk for childhood onset asthma. These and other genetic findings are providing a list of well‐validated asthma and allergy susceptibility genes that are expanding our understanding of the common and unique biological pathways that are dysregulated in these related conditions. Ongoing studies will continue to broaden our understanding of asthma and allergy and unravel the mechanisms for the development of these complex traits.
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The discrepancy in clinical impact may be due to broader mechanisms impacting allergic disease, such as the role of microbial diversity and environmental interactions.
“This discrepancy may be due to broader mechanisms impacting allergic disease. One such mechanism includes the role of microbial diversity and environmental interactions (66).”
From Indoor Allergen Interventions in Homes and Schools for Managing Asthma (2025) · cites this paper as [66]
The “Environment modifiers of asthma and allergy” section describes environmental exposures, including microbial exposures, as potential modifiers of asthma and allergy risk. It does not specifically discuss microbial diversity or establish its role as a mechanism; the authors say those mechanisms need further study. No page number is available in our copy. (LLM, conf=0.82)
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- Authors
- Ober, C., & Yao, T.
- Affiliations
- University of Chicago (US)
- Chang Gung University (TW)
- Corresponding author
- Ober, Carole
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2011-06-20
- Volume
- 242
- Issue
- 1
- Pages
- 10-30
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- PMC
- PMC3151648
- OpenAlex
- W1808276465
- Cited by
- 698
- References
- 287
- Citations by year
- 2026: 32 · 2025: 46 · 2024: 33 · 2023: 38 · 2022: 42 · 2021: 46 · 2020: 46 · 2019: 53 · 2018: 58 · 2017: 47 · 2016: 54 · 2015: 57 · 2014: 56 · 2013: 50 · 2012: 33
- FWCI
- 4.93
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Immunological Reviews (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL101543, RC2HL101651, HL85197, HL 70831, HL101651, RC2HL101543, R01HL085197, P01HL070831)
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- asthma genetics, allergic diseases, genome-wide association study, IL-33, thymic stromal lymphopoietin, ST2, innate immunity, Th2 cells, ORMDL3, childhood asthma, susceptibility genes, cytokines
- MeSH terms
- Interleukin-33, Interleukin-1 Receptor-Like 1 Protein, Gasdermins, Thymic Stromal Lymphopoietin, Adult, Asthma, Child, Chromosomes, Human, Pair 17, Gene Expression Regulation, Humans, Hypersensitivity, Immediate, Immunity, Innate, Infant, Interleukins, Genetic Linkage, Lymphocyte Activation, Membrane Proteins, Neoplasm Proteins, Receptors, Cell Surface, Genetic Variation, Meta-Analysis as Topic, Cytokines, Th2 Cells, Genetic Predisposition to Disease, Genome-Wide Association Study, Genetic Loci
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