What you carry at this position in your DNA and what research says about it.
Asthma and Allergy Risk: 6/10 evidence, 55 publications.
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Sample genotype (not yours): C/C
Typical Risk of Asthma and Allergies
This genotype is associated with baseline levels of interleukin 13 expression. It provides relative protection against the elevated inflammatory risks seen in T allele carriers.
What this genotype means: Standard baseline risk for asthma; Typical lung function decline with smoking.
Sample genotype (not yours): C/T
Increased Risk of Asthma and Allergies
Carrying one copy of the T allele increases interleukin 13 expression, elevating the risk of inflammatory and atopic conditions.
What this genotype means: Elevated risk of developing asthma; Higher susceptibility to allergic rhinitis and eczema.
Sample genotype (not yours): T/T
Highest Risk of Asthma and Accelerated Lung Decline
Two copies of the T allele lead to the highest levels of interleukin 13, significantly raising allergy risks and making lungs highly sensitive to tobacco smoke.
What this genotype means: Highest genetic risk for asthma and eczema; Pronounced lung function decline from smoking; Increased risk of sunitinib side effects.
Gene function and biological role
Gene Function: The IL13 gene encodes interleukin 13, an immunoregulatory cytokine primarily produced by activated T helper type 2 cells. This cytokine acts as a critical mediator in the pathogenesis of allergic asthma, tissue remodeling, and mucosal inflammatory responses. Elevated levels of interleukin 13 drive airway hyperreactivity, mucus hypersecretion, and immunoglobulin E production [1]. Genetic variations within this gene can alter its expression levels, directly influencing susceptibility to chronic inflammatory and atopic diseases [2].
Variant Impact: This variant, rs1800925, is located in the 5 prime untranslated promoter region of the IL13 gene, where it directly influences transcription factor binding and gene expression. The T allele increases promoter activity, leading to higher production of interleukin 13 and promoting a pro-inflammatory state [3]. This elevated expression is strongly associated with heightened susceptibility to asthma and allergic rhinitis [4]. Additionally, the variant alters the lungs' vulnerability to environmental stressors, such as cigarette smoke [5].
Key Insight: The T allele acts like an volume booster for inflammation, increasing the production of interleukin 13 and making the airways and skin significantly more sensitive to environmental triggers.
Location: IL13. Chromosome 5 · 5q31.1 · 132.7 Mb
Origin Story: The pro-inflammatory T allele is thought to have been maintained in certain populations because an active Th2 immune response enhances natural resistance to parasitic worm infections, such as schistosomes.
Estimated prevalence by population
Global 55.7%; European 63.1%; African 36.7%; East Asian 69.0%; South Asian 61.8%; Americas 60.7%; Ashkenazi 59.3%; Finnish 62.9%; Middle Eastern 52.5%; Amish 78.6%.
Estimated CC genotype frequency.
Global 36.9%; European 32.7%; African 47.7%; East Asian 28.2%; South Asian 33.6%; Americas 34.4%; Ashkenazi 35.4%; Finnish 32.8%; Middle Eastern 39.9%; Amish 20.1%.
Estimated CT genotype frequency.
Global 7.4%; European 4.2%; African 15.5%; East Asian 2.9%; South Asian 4.6%; Americas 4.9%; Ashkenazi 5.3%; Finnish 4.3%; Middle Eastern 7.6%; Amish 1.3%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Organ Systems
Respiratory Health
Asthma. Evidence: 4/10. Source: PMID 33191717. Typical Risk.
Smoking-Related Lung Decline. Evidence: 3/10. Source: PMID 29381928. Typical Decline.
Skin & Hair Conditions
Atopic Eczema. Evidence: 6/10. Source: PMID 35577104. Typical Risk.
Immunity & Inflammation
Allergy & Hypersensitivity
Allergic Rhinitis. Evidence: 4/10. Source: PMID 22750299. Typical Risk.
Pharmacogenomics
Chemotherapy Response
Sunitinib Toxicity. Evidence: 5/10. Source: PMID 26387812. Typical Response.
Showing effects for C/T genotype
Asthma. Evidence: 4/10. Source: PMID 33191717. Increased Risk.
Atopic Eczema. Evidence: 6/10. Source: PMID 35577104. Increased Risk.
Allergic Rhinitis. Evidence: 4/10. Source: PMID 22750299. Increased Risk.
Showing effects for T/T genotype
Asthma. Evidence: 4/10. Source: PMID 33191717. Highest Risk.
Smoking-Related Lung Decline. Evidence: 3/10. Source: PMID 29381928. Accelerated Decline.
Atopic Eczema. Evidence: 6/10. Source: PMID 35577104. Highest Risk.
Allergic Rhinitis. Evidence: 4/10. Source: PMID 22750299. Highest Risk.
Sunitinib Toxicity. Evidence: 5/10. Source: PMID 26387812. Increased Toxicity.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Having two copies of the common C allele is associated with standard baseline levels of interleukin 13 production. Large-scale genetic analyses indicate that this genotype carries a typical, non-elevated risk for developing asthma [1] and allergic rhinitis [2]. In the presence of environmental triggers like cigarette smoke, individuals with this genotype experience a standard, gradual decline in lung function over time rather than an accelerated loss [3]. Furthermore, studies on skin health show no elevated genetic predisposition to atopic eczema or related inflammatory skin conditions for this group [4]. If treated with the cancer medication sunitinib, this genotype is associated with a standard tolerability profile [5].
Standard baseline risk for asthma; Typical lung function decline with smoking.
Sample genotype: CT (Heterozygous)
Carrying one copy of the inflammatory T allele is associated with increased promoter activity of the IL13 gene. This molecular change leads to higher circulating levels of interleukin 13, which primes the immune system toward allergic responses. Clinical studies and meta-analyses show that this heterozygous genotype significantly increases the risk of developing asthma [1] and allergic rhinitis [2]. There is also an elevated susceptibility to skin barrier inflammation, specifically atopic eczema [3]. When exposed to cigarette smoke, individuals with this genotype show a standard rate of lung function decline, similar to the common homozygous genotype [4]. However, the overall tendency toward Th2-mediated inflammation remains elevated compared to non-carriers.
Elevated risk of developing asthma; Higher susceptibility to allergic rhinitis and eczema.
Sample genotype: TT (Homozygous)
Carrying two copies of the T allele results in the highest promoter activity and maximum expression of the pro-inflammatory cytokine interleukin 13. This genotype is strongly linked to a heightened risk of asthma [1] and severe allergic rhinitis [2]. Lung function is particularly sensitive to environmental toxins in this group; research shows that long-term smokers with this genotype experience an accelerated 8.2% reduction in lung capacity per 20 pack-years, compared to only 2.4% in other genotypes [3]. There is also a significantly higher risk of developing atopic eczema [4]. Additionally, if prescribed the chemotherapy drug sunitinib, this genotype is associated with an increased risk of severe drug toxicity and low white blood cell counts [5].
Highest genetic risk for asthma and eczema; Pronounced lung function decline from smoking; Increased risk of sunitinib side effects.
Variants with shared genetic architecture
rs20541 · IL13 Gene · Chr 5 · Asthma and Eczema Risk
rs848 · IL13 Gene · Chr 5 · Asthma and Eczema
rs1295686 · IL13 Gene · Chr 5 · Asthma and Eczema Risk
Interleukin 13 gene polymorphism and susceptibility to asthma: a meta-regression and meta-analysis.
IL-13 polymorphisms contribute to the risk of asthma: a meta-analysis.
Content updated August 2026.
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