What you carry at this position in your DNA and what research says about it.
Autoimmune Disease Risk: 10/10 evidence, 75 publications.
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Sample genotype (not yours): G/G
Typical Autoimmune Disease Risk
A standard baseline risk for inflammatory bowel and skin conditions characterizes this profile. There is no elevated risk compared to the general population, but the protective effect of the rare variant is absent.
What this genotype means: Standard baseline risk for Crohn's disease; Standard baseline risk for ulcerative colitis; Standard baseline risk for psoriasis.
Sample genotype (not yours): A/A
Significantly Lower Autoimmune Risk
Two copies of the rare variant provide exceptional protection against several chronic inflammatory diseases. This includes a substantially reduced risk of Crohn's disease, ulcerative colitis, and psoriasis.
What this genotype means: Nearly 4x lower risk of Crohn's disease; Nearly 3x lower risk of ulcerative colitis; Robust protection against psoriasis and ankylosing spondylitis.
Sample genotype (not yours): G/A
One copy of the rare variant provides strong protection against several chronic inflammatory diseases. This includes a substantially reduced risk of Crohn's disease, ulcerative colitis, and psoriasis.
What this genotype means: Nearly 4x lower risk of Crohn's disease; Nearly 3x lower risk of ulcerative colitis; Reduced risk of psoriasis and ankylosing spondylitis.
Gene function and biological role
Gene Function: The IL23R gene encodes a subunit of the receptor for interleukin-23, a key pro-inflammatory cytokine. This receptor is expressed on the surface of several immune cells, including T-helper 17 cells, which play a central role in coordinating inflammatory responses. When interleukin-23 binds to its receptor, it triggers a signaling cascade that promotes the survival and proliferation of these inflammatory cells. Overactivity of this pathway is a major driver of chronic inflammation and tissue damage in various organs. Consequently, genetic variations that alter the structure or abundance of this receptor can significantly influence susceptibility to autoimmune and inflammatory disorders.
Variant Impact: A missense mutation at rs11209026 in the IL23R gene changes the amino acid arginine to glutamine at position 381 of the receptor protein. This specific structural change, often referred to as p.Arg381Gln or R381Q, occurs in a region of the receptor that is crucial for its signaling function. The altered glutamine-carrying receptor exhibits a reduced capacity to transmit inflammatory signals when stimulated by interleukin-23. This dampening of the interleukin-23 pathway leads to decreased production of downstream inflammatory cytokines like interleukin-17. As a result, this functional change acts as a natural brake on the immune system, protecting carriers from hyper-inflammatory states.
Key Insight: Unlike most disease-associated genetic variants that increase risk, the minor variant of this SNP is highly protective, acting as a natural shield against several severe autoimmune conditions. This protective effect is so pronounced that it has inspired the development of modern therapeutic drugs designed to mimic its signal-dampening behavior.
Location: IL23R. Chromosome 1 · 1p31.3 · 67.2 Mb
Estimated prevalence by population
Global 91.1%; European 87.2%; African 97.5%; East Asian 99.9%; South Asian 97.3%; Americas 90.1%; Ashkenazi 86.3%; Finnish 88.4%; Middle Eastern 91.4%; Amish 80.6%.
Estimated GG genotype frequency.
Global 8.6%; European 12.4%; African 2.5%; East Asian 0.1%; South Asian 2.7%; Americas 9.7%; Ashkenazi 13.2%; Finnish 11.3%; Middle Eastern 8.4%; Amish 18.3%.
Estimated GA genotype frequency.
Global 0.3%; European 0.4%; African < 0.1%; East Asian < 0.1%; South Asian < 0.1%; Americas 0.3%; Ashkenazi 0.5%; Finnish 0.4%; Middle Eastern 0.2%; Amish 1.0%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Immunity & Inflammation
Chronic Inflammatory Diseases
Crohn's Disease. Evidence: 10/10. Source: PMID 17068223. Typical Risk.
Ulcerative Colitis. Evidence: 8/10. Source: PMID 19122664. Typical Risk.
Autoimmune Diseases
Ankylosing Spondylitis. Evidence: 8/10. Source: PMID 20062062. Typical Risk.
Organ Systems
Skin & Hair Conditions
Psoriasis. Evidence: 7/10. Source: PMID 17587057. Typical Risk.
Pharmacogenomics
Adverse Drug Reactions
Drug-Induced Psoriasis. Evidence: 8/10. Source: PMID 26194362. Typical Risk.
Showing effects for A/A genotype
Crohn's Disease. Evidence: 10/10. Source: PMID 17068223. ~4x Lower Risk.
Ulcerative Colitis. Evidence: 8/10. Source: PMID 19122664. ~3x Lower Risk.
Ankylosing Spondylitis. Evidence: 8/10. Source: PMID 20062062. ~1.6x Lower Risk.
Psoriasis. Evidence: 7/10. Source: PMID 17587057. ~1.6x Lower Risk.
Showing effects for G/A genotype
Drug-Induced Psoriasis. Evidence: 8/10. Source: PMID 26194362. Increased Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Two copies of the major G allele represent the most common genetic profile globally, occurring in over 95% of people. This genotype produces fully functional interleukin-23 receptors that respond normally to inflammatory signals. Because these receptors are fully active, they maintain a standard level of immune surveillance and defense against pathogens. However, this also means you do not benefit from the strong protective shield against autoimmune diseases seen in carriers of the rare A allele. Your risk for conditions like Crohn's disease, ulcerative colitis, and psoriasis remains at the typical population baseline. Maintaining a healthy lifestyle and supporting gut microbiome health are standard ways to manage overall inflammatory risk.
Standard baseline risk for Crohn's disease; Standard baseline risk for ulcerative colitis; Standard baseline risk for psoriasis.
Sample genotype: AA (Homozygous)
Double copies of the protective A allele represent an extremely rare genetic profile, found in less than 1% of most populations. With this genotype, all of your interleukin-23 receptors carry the structural change that significantly dampens inflammatory signaling. This complete shift in receptor function provides a highly robust natural shield against hyper-inflammatory autoimmune disorders. Clinical data indicates that this profile is associated with a nearly four-fold lower risk of developing Crohn's disease. The risk for ulcerative colitis is also reduced by approximately three-fold, and the risks for psoriasis and ankylosing spondylitis are similarly minimized. Because this genotype is so rare, most clinical studies group it with the heterozygous genotype when evaluating health outcomes. Overall, this profile represents one of the strongest genetic protective factors known for inflammatory bowel and skin diseases.
Nearly 4x lower risk of Crohn's disease; Nearly 3x lower risk of ulcerative colitis; Robust protection against psoriasis and ankylosing spondylitis.
Sample genotype: GA (Heterozygous)
Possessing one copy of the protective A allele means about half of the interleukin-23 receptors have a structural change that dampens inflammatory signaling. This natural reduction in signaling acts as a powerful shield against hyper-inflammatory autoimmune disorders. Large-scale genetic studies show that carriers of this genotype have a nearly four-fold lower risk of developing Crohn's disease. Similarly, the risk for ulcerative colitis is reduced by approximately three-fold, and the risks for psoriasis and ankylosing spondylitis are also significantly lowered. However, some research suggests that if you are treated with TNF-alpha inhibitors, you may have a slightly higher chance of developing a paradoxical skin reaction. Overall, this genetic profile is highly advantageous for long-term inflammatory health.
Nearly 4x lower risk of Crohn's disease; Nearly 3x lower risk of ulcerative colitis; Reduced risk of psoriasis and ankylosing spondylitis.
Variants with shared genetic architecture
rs7517847 · IL23R Gene · Chr 1 · Crohn Disease Risk
rs11465804 · IL23R Gene · Chr 1 · Inflammatory Disease Risk
rs1004819 · IL23R Gene · Chr 1 · Crohn's Disease Risk
Content updated August 2026.
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