IL1RL1 rs1041973: What Your Genotype Means
The rs1041973 variant is a genetic change located within the IL1RL1 gene, which plays a role in the body's immune signaling pathways. Research has associated the A allele of this variant with increased production of IL-5, a cytokine involved in allergic inflammation.
What each genotype means
Increased allergic inflammation potential
Research indicates that the A allele is positively associated with increased production of IL-5, a cytokine involved in allergic inflammation. Carriers of this genotype may show higher levels of specific IgE and sensitivity to certain allergens, though these associations are based on limited evidence and can vary by population. Please discuss any concerns regarding allergic symptoms or immune health with your clinician.
This is a common genotype found across many global populations.
Intermediate allergic inflammation potential
This genotype represents a heterozygous state for the IL1RL1 variant. Studies suggest that the A allele is linked to increased IL-5 production and allergic markers, and carrying one copy may result in an intermediate influence on these inflammatory pathways compared to those with two A alleles. As this evidence is limited, please consult with your healthcare provider regarding any personal history of allergies or asthma.
This is a common genotype found across many global populations.
Baseline allergic inflammation profile
This genotype represents the absence of the A allele associated with increased IL-5 production in this specific IL1RL1 variant. Research suggests that individuals with this genotype do not carry the specific genetic association linked to elevated allergic inflammation markers observed with the A allele. Please note that allergic conditions are complex and influenced by many genetic and environmental factors; discuss any health concerns with your clinician.
This is a common genotype found across many global populations.
Understanding the rs1041973 Variant
The rs1041973 variant is a single nucleotide polymorphism (SNP) situated within the IL1RL1 gene on chromosome 2. In genetics, a SNP represents a variation at a single position in the DNA sequence among individuals. This specific variant has been identified in scientific literature as a potential regulatory factor for the expression of the IL1RL1 gene. Because it is located in a region that influences how genes are turned on or off, researchers study it to understand how subtle differences in our genetic code might contribute to variations in immune system activity. It is important to note that while this variant is documented in genomic databases, its presence is just one of many factors that influence human biology and health.
The Role of the IL1RL1 Gene
The IL1RL1 gene provides instructions for making a protein known as ST2, which acts as a receptor for IL-33, a signaling molecule in the immune system. This receptor is primarily found on the surface of specific immune cells, including T helper-2 (Th2) cells and mast cells. When IL-33 binds to the ST2 receptor, it triggers a cascade of immune responses, including the release of cytokines like IL-4, IL-5, and IL-13. These cytokines are essential for the body's defense, but they are also key drivers of allergic inflammation. By regulating the sensitivity of immune cells to IL-33, the IL1RL1 gene helps modulate the intensity of the body's inflammatory response to various environmental triggers.
Research and Evidence Strength
Scientific research into rs1041973 has primarily focused on its association with immune-related traits. Studies, such as those conducted in Brazilian populations, have observed that the A allele is positively associated with higher levels of IL-5 production and increased sensitivity to certain allergens. Additionally, some evidence suggests this variant may influence the levels of soluble ST2 (sST2) in the blood. However, the evidence strength for these associations is currently considered limited. Most findings come from specific population studies, and the biological mechanisms are complex, involving multiple genetic and environmental factors. Because these associations are based on statistical correlations rather than direct causation, more large-scale, diverse research is required to fully understand the clinical significance of this variant.
Population Frequency
The rs1041973 variant is considered a common genetic polymorphism, meaning it is found at significant frequencies across various human populations. While specific allele frequencies can vary depending on ancestral background, it is widely distributed, allowing researchers to study its effects in diverse groups. The prevalence of the A and G alleles is documented in large-scale genomic databases, which provide the baseline data necessary for genome-wide association studies (GWAS) to identify potential links between this SNP and various immune-related traits.
Interpreting Your Genetic Information
If you have received information about your rs1041973 genotype, it is important to view it within the context of current scientific understanding. This information is intended for educational purposes and does not constitute a medical diagnosis or a prediction of health outcomes. Genetic variants like rs1041973 are only one piece of a much larger puzzle that includes your environment, lifestyle, and other genetic factors. You cannot use this information to make medical decisions or change treatments on your own. If you have concerns about allergies, inflammation, or your immune health, please consult with a qualified healthcare professional or an immunologist who can interpret your health history alongside any genetic data you may have.
How common is this variant?
The rs1041973 variant is a common polymorphism found across diverse global populations, with both the A and G alleles appearing at significant frequencies.
Frequently asked questions
Is rs1041973 a cause of asthma?
No, rs1041973 is not a direct cause of asthma. While some studies have found statistical associations between this variant and allergic traits, asthma is a complex condition influenced by many genes and environmental factors.
Can I use this SNP to predict my allergy risk?
No, you cannot use this SNP to predict your risk of developing allergies. Genetic associations are statistical in nature and do not provide a definitive medical prediction for an individual.
What should I do if I have the A allele?
The presence of the A allele is a common genetic finding and does not require specific medical action. If you have concerns about your immune health or allergies, you should discuss them with your doctor.
Where can I find more information on IL1RL1?
You can find reliable information on the IL1RL1 gene through resources like the NIH's MedlinePlus Genetics or the OMIM database. These sites provide comprehensive summaries of gene functions and related research.
Sources & further reading
Educational information only, last refreshed 9/15/2026. Not medical advice — these associations describe population statistics, not individual predictions.
Curious what your genotype is for rs1041973?
Upload a raw DNA file from 23andMe, AncestryDNA, MyHeritage, or FamilyTreeDNA and see this variant — plus thousands more — interpreted in your full report.
Get my report — $29Related variants in IL1RL1
This variant in the IL1RL1/IL18R1 locus influences ST2 receptor expression and modifies individual susceptibility to allergic sensitization and asthma.
An intergenic regulatory variant upstream of IL1RL1 that influences circulating soluble ST2 levels and severity of allergic rhinitis.
Intronic regulatory variant in the IL1RL1/IL18R1 cluster modulating ST2 receptor expression and inflammatory disease risk.
ST2/interleukin-1 receptor-like 1 variant associated with altered IL-33 signaling and heightened risk for allergic asthma and atopy.
A regulatory variant within the IL1RL1 (ST2) gene locus associated with allergic rhinitis, eosinophil count regulation, and atopic asthma susceptibility.
Intronic regulatory SNP in IL1RL1/ST2 associated with sST2 expression levels and susceptibility to allergic sensitization and asthma.