What you carry at this position in your DNA and what research says about it.
Asthma and Allergy Risk: 8/10 evidence, 16 publications.
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Sample genotype (not yours): C/C
Typical Asthma and Allergy Risk
Two copies of the C allele are associated with typical levels of blood eosinophils and a standard risk of developing asthma. This genotype supports normal production of the protective decoy receptor that helps regulate airway inflammation.
What this genotype means: Typical baseline risk of asthma and allergies; Standard levels of blood eosinophils; Normal production of protective decoy receptors.
Sample genotype (not yours): C/T
Slightly Increased Asthma and Allergy Risk
Carrying one copy of the T allele is linked to slightly higher blood eosinophil counts and a modest increase in the risk of asthma. This is due to a slight reduction in the protective decoy receptor that controls airway inflammation.
What this genotype means: Slightly elevated risk of asthma; Mildly higher blood eosinophil levels; Slightly increased susceptibility to nasal polyps.
Sample genotype (not yours): T/T
Increased Asthma and Allergy Risk
Two copies of the T allele are associated with significantly higher blood eosinophil counts and an elevated risk of asthma. This genotype leads to lower levels of the protective decoy receptor, allowing more airway inflammation.
What this genotype means: Elevated risk of asthma and allergic inflammation; Higher baseline blood eosinophil counts; Increased risk of nasal polyps.
Gene function and biological role
Gene Function: The IL1RL1 gene encodes the interleukin-1 receptor-like 1 protein, also known as ST2, which plays a critical role in immune system regulation. This protein exists in two main forms: a membrane-bound receptor that transmits inflammatory signals and a soluble decoy receptor that neutralizes them. The soluble form acts as a molecular sponge, binding to and blocking the inflammatory cytokine interleukin-33. By regulating interleukin-33 activity, this gene serves as a central controller of type 2 immune responses, which drive allergic reactions and airway inflammation. Variations in this gene can alter the balance of these receptor forms, directly influencing susceptibility to inflammatory and respiratory diseases.
Variant Impact: The rs1420101 variant is an intron variant located within the IL1RL1 gene that influences gene expression. This genetic change acts as an expression quantitative trait locus, altering how much soluble decoy receptor is produced in airway epithelial cells. The T allele is associated with lower expression of the protective decoy receptor, leaving more active interleukin-33 to trigger immune pathways. This reduction in decoy receptor levels leads to heightened airway inflammation and elevated levels of eosinophils, a type of white blood cell involved in allergic responses. Consequently, this variant is a well-established genetic marker for respiratory and allergic conditions.
Key Insight: The soluble form of the protein encoded by this gene acts as a molecular sponge, soaking up inflammatory signals before they can trigger allergic reactions.
Location: IL1RL1. Chromosome 2 · 2q12.1 · 102.3 Mb
Estimated prevalence by population
Global 41.9%; European 38.6%; African 44.2%; East Asian 31.7%; South Asian 40.7%; Americas 50.1%; Ashkenazi 47.5%; Finnish 46.2%; Middle Eastern 21.0%; Amish 52.8%.
Estimated CC genotype frequency.
Global 45.5%; European 47.1%; African 44.6%; East Asian 49.2%; South Asian 46.2%; Americas 41.4%; Ashkenazi 42.8%; Finnish 43.5%; Middle Eastern 49.7%; Amish 39.7%.
Estimated CT genotype frequency.
Global 12.7%; European 14.3%; African 11.2%; East Asian 19.1%; South Asian 13.1%; Americas 8.5%; Ashkenazi 9.6%; Finnish 10.3%; Middle Eastern 29.3%; Amish 7.5%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Organ Systems
Respiratory Health
Asthma. Evidence: 8/10. Source: PMID 30578877. Typical Risk.
Nasal Polyps. Evidence: 6/10. Source: PMID 30643255. Typical Risk.
Cardiovascular & Metabolic
Blood Cell & Iron Traits
Eosinophil Count. Evidence: 9/10. Source: PMID 19198610. Typical Levels.
Immunity & Inflammation
Inflammatory & Circulating Protein Markers
Decoy Receptor Levels. Evidence: 6/10. Source: PMID 28369058. Higher Levels.
Showing effects for C/T genotype
Asthma. Evidence: 8/10. Source: PMID 30578877. ~1.11x Risk.
Nasal Polyps. Evidence: 6/10. Source: PMID 30643255. ~1.15x Risk.
Eosinophil Count. Evidence: 9/10. Source: PMID 19198610. ~6.4% Higher.
Decoy Receptor Levels. Evidence: 6/10. Source: PMID 28369058. Typical Levels.
Showing effects for T/T genotype
Asthma. Evidence: 8/10. Source: PMID 30578877. ~1.23x Risk.
Nasal Polyps. Evidence: 6/10. Source: PMID 30643255. ~1.32x Risk.
Eosinophil Count. Evidence: 9/10. Source: PMID 19198610. ~12.8% Higher.
Decoy Receptor Levels. Evidence: 6/10. Source: PMID 28369058. Lower Levels.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
A homozygous C/C genetic profile is associated with higher levels of the soluble decoy receptor sST2, which binds and neutralizes the inflammatory cytokine IL-33. By keeping IL-33 in check, the immune system maintains a more balanced, typical response to environmental triggers. Baseline blood eosinophil counts remain within the normal range compared to T allele carriers. This translates to a lower, typical susceptibility to asthma and related respiratory conditions. Additionally, the risk of developing nasal polyps or chronic sinus inflammation remains at the standard population baseline. Airway tissues are less prone to the overactive type 2 allergic inflammation that characterizes allergic diseases. Overall, this genetic profile supports healthy airway function and a lower likelihood of respiratory hypersensitivity.
Typical baseline risk of asthma and allergies; Standard levels of blood eosinophils; Normal production of protective decoy receptors.
Sample genotype: CT (Heterozygous)
A heterozygous C/T genetic profile is associated with a moderate reduction in the expression of the soluble decoy receptor sST2 in the lungs. With fewer decoy receptors available to neutralize the inflammatory cytokine IL-33, the immune system may react more strongly to environmental allergens. This often manifests as a slight increase in peripheral blood eosinophil counts. Clinical data associates this genotype with a modestly elevated risk of developing asthma, with an odds ratio of approximately 1.11 per risk allele. There is also a slightly higher susceptibility to nasal polyps and chronic sinus issues. Although this represents only a minor increase in overall risk, it highlights a genetic tendency toward heightened allergic sensitivity. Most individuals with this genotype do not develop severe respiratory conditions unless exposed to strong environmental triggers.
Slightly elevated risk of asthma; Mildly higher blood eosinophil levels; Slightly increased susceptibility to nasal polyps.
Sample genotype: TT (Homozygous)
A homozygous T/T genetic profile is strongly linked to a type 2-high inflammatory profile. Research demonstrates that this genotype results in significantly lower levels of the soluble decoy receptor sST2. Because sST2 normally acts as a molecular sponge to neutralize the inflammatory cytokine IL-33, its deficiency allows IL-33 to drive unchecked allergic pathways. This molecular environment leads to a notable increase in blood eosinophil counts, which are key cellular drivers of allergic responses. Clinical studies show that this genotype is associated with an elevated risk of developing asthma and experiencing more severe respiratory symptoms. There is also a well-documented increase in the risk of nasal polyps and chronic rhinosinusitis. This genetic insight can help explain a stronger biological tendency toward allergic and respiratory hypersensitivity.
Elevated risk of asthma and allergic inflammation; Higher baseline blood eosinophil counts; Increased risk of nasal polyps.
Variants with shared genetic architecture
rs34290285 · D2HGDH Gene · Chr 2 · Asthma and Allergy Risk
rs1800925 · IL13 Gene · Chr 5 · Asthma and Allergy Risk
rs1143633 · IL1B Gene · Chr 2 · Allergy and Joint Health
Content updated August 2026.
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