What you carry at this position in your DNA and what research says about it.
Autoimmune Disease Risk: 8/10 evidence, 39 publications.
You're viewing every possible genotype for this variant.
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Sample genotype (not yours): G/G
Higher Diabetes Risk but Lower Bowel Inflammation Risk
This genotype is associated with a slightly higher risk of type 1 diabetes but offers protection against inflammatory bowel diseases.
What this genotype means: Slightly increased risk of type 1 diabetes; Decreased risk of inflammatory bowel disease; Decreased risk of systemic lupus erythematosus.
Sample genotype (not yours): A/A
Higher Bowel Inflammation Risk but Lower Diabetes Risk
This genotype is linked to a higher risk of inflammatory bowel diseases but provides protection against type 1 diabetes.
What this genotype means: Slightly increased risk of inflammatory bowel disease; Slightly increased risk of systemic lupus erythematosus; Decreased risk of type 1 diabetes.
Sample genotype (not yours): G/A
Typical Risk for Autoimmune and Inflammatory Conditions
This genotype represents a balanced genetic baseline with typical risks for both diabetes and inflammatory bowel diseases.
What this genotype means: Typical risk of type 1 diabetes; Typical risk of inflammatory bowel disease; Typical risk of systemic lupus erythematosus.
Gene function and biological role
Gene Function: The IL10 gene encodes interleukin-10, a powerful anti-inflammatory cytokine that serves as a master regulator of the immune system. It is produced by various immune cells, including B cells and T cells, to limit inflammatory responses and maintain tissue homeostasis. By inhibiting the synthesis of pro-inflammatory cytokines, interleukin-10 prevents excessive immune-mediated tissue damage. Dysregulation of IL10 expression is heavily implicated in the pathogenesis of multiple autoimmune and chronic inflammatory disorders.
Variant Impact: The rs3024505 variant is a single nucleotide polymorphism located in an intergenic region downstream of the IL10 gene. This non-coding variant resides within an enhancer region that influences the transcription and expression levels of interleukin-10. The G and A alleles alter the binding of transcription factors, thereby modulating how much anti-inflammatory cytokine is produced during an immune response. Because it acts as a molecular dial for inflammation, this variant represents a key genetic link between distinct autoimmune pathways.
Key Insight: This variant acts as an evolutionary trade-off, where the allele that increases the risk of inflammatory bowel disease actually protects against type 1 diabetes.
Location: IL10. Chromosome 1 · 1q32.1 · 206.8 Mb
Origin Story: The geographic distribution of these alleles suggests that historical exposure to diverse parasites and pathogens shaped the genetic selection of IL10 variants to balance active immune defense with self-tolerance.
Estimated prevalence by population
Global 79.1%; European 71.1%; African 91.0%; East Asian 95.0%; South Asian 79.4%; Americas 84.4%; Ashkenazi 74.9%; Finnish 69.4%; Middle Eastern 75.2%; Amish 78.9%.
Estimated GG genotype frequency.
Global 19.4%; European 26.4%; African 8.8%; East Asian 4.9%; South Asian 19.4%; Americas 15.0%; Ashkenazi 23.3%; Finnish 27.8%; Middle Eastern 23.0%; Amish 19.9%.
Estimated GA genotype frequency.
Global 1.5%; European 2.5%; African 0.2%; East Asian 0.1%; South Asian 1.2%; Americas 0.7%; Ashkenazi 1.8%; Finnish 2.8%; Middle Eastern 1.8%; Amish 1.2%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Immunity & Inflammation
Chronic Inflammatory Diseases
Inflammatory Bowel Disease. Evidence: 8/10. Source: PMID 23128233. Lower Risk.
Autoimmune Diseases
Lupus. Evidence: 8/10. Source: PMID 19838195. Lower Risk.
Cardiovascular & Metabolic
Diabetes & Glycemic Traits
Type 1 Diabetes. Evidence: 8/10. Source: PMID 19430480. ~1.14x Higher Risk.
Showing effects for A/A genotype
Inflammatory Bowel Disease. Evidence: 8/10. Source: PMID 23128233. ~1.2x Higher Risk.
Lupus. Evidence: 8/10. Source: PMID 19838195. ~1.18x Higher Risk.
Type 1 Diabetes. Evidence: 8/10. Source: PMID 19430480. Lower Risk.
Showing effects for G/A genotype
Inflammatory Bowel Disease. Evidence: 8/10. Source: PMID 23128233. Typical Risk.
Lupus. Evidence: 8/10. Source: PMID 19838195. Typical Risk.
Type 1 Diabetes. Evidence: 8/10. Source: PMID 19430480. Typical Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
A homozygous G/G profile is associated with a higher risk of developing type 1 diabetes. Conversely, this same genetic profile appears to offer protection against several inflammatory bowel conditions, including ulcerative colitis and Crohn's disease. Large-scale genomic studies demonstrate that the G allele correlates with a lower likelihood of systemic lupus erythematosus. This creates an evolutionary trade-off where a heightened risk for one autoimmune condition is balanced by a reduced susceptibility to others. The biological mechanism involves subtle changes in interleukin-10 expression, which alters how the immune system regulates self-tolerance and gut inflammation. While the elevated risk of type 1 diabetes is notable, environmental factors and overall lifestyle play a major role in actual disease development. Understanding this genetic baseline helps clarify how the body's inflammatory pathways are naturally balanced.
Slightly increased risk of type 1 diabetes; Decreased risk of inflammatory bowel disease; Decreased risk of systemic lupus erythematosus.
Sample genotype: AA (Homozygous)
A homozygous A/A profile is linked to an increased susceptibility to inflammatory bowel diseases, including Crohn's disease and ulcerative colitis. This genetic makeup is also associated with a higher risk of systemic lupus erythematosus. However, the same A/A genotype provides a protective effect against the development of type 1 diabetes. This represents a classic evolutionary trade-off where susceptibility to gut inflammation is balanced by resistance to pancreatic autoimmunity. The underlying biology relates to altered interleukin-10 regulation, which can lead to heightened inflammatory responses in the digestive tract. While these genetic risks are elevated, they do not guarantee the onset of any condition, as diet and gut microbiome composition are critical co-factors. This profile highlights the complex, dual-sided nature of immune system genetics.
Slightly increased risk of inflammatory bowel disease; Slightly increased risk of systemic lupus erythematosus; Decreased risk of type 1 diabetes.
Sample genotype: GA (Heterozygous)
An intermediate G/A genotype represents a balanced genetic baseline for autoimmune risks. Having one copy of each allele means the risks for both type 1 diabetes and inflammatory bowel diseases are close to the population average. Studies show that this heterozygous state does not strongly lean toward either extreme of the autoimmune spectrum. The immune system maintains a moderate level of interleukin-10 production, avoiding the severe imbalances associated with the homozygous states. This typical profile is common in most populations and represents a standard evolutionary compromise. It provides a neutral baseline where neither the protective benefits nor the elevated risks of either allele are fully pronounced. Overall, this genotype is considered a typical reference point for immune wellness.
Typical risk of type 1 diabetes; Typical risk of inflammatory bowel disease; Typical risk of systemic lupus erythematosus.
Variants with shared genetic architecture
rs3024493 · IL10 Gene · Chr 1 · Ulcerative Colitis Risk
rs1800871 · IL10 Gene · Chr 1 · Inflammatory Disease Risk
rs1518111 · IL10 Gene · Chr 1 · Behçet's Disease Risk
Content updated August 2026.
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