What you carry at this position in your DNA and what research says about it.
Autoimmune Disease Risk: 5/10 evidence, 47 publications.
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Sample genotype (not yours): C/C
Typical Bowel Risk but Higher Graves Disease Risk
Typical baseline risk is associated with this genotype for inflammatory bowel diseases like Crohn's and ulcerative colitis. However, it carries an approximately 2.3-fold increased risk for Graves' disease.
What this genotype means: Typical risk for Crohn's disease and ulcerative colitis; Increased risk for Graves' disease and thyroid-related inflammation.
Sample genotype (not yours): A/A
Increased Bowel Risk but Typical Graves Disease Risk
Increased risk for chronic inflammatory bowel conditions is paired with a typical baseline risk for Graves' disease here. It represents a 1.5-fold higher risk for Crohn's disease.
What this genotype means: Increased risk for Crohn's disease and ulcerative colitis; Higher susceptibility to ankylosing spondylitis; Typical baseline risk for Graves' disease.
Sample genotype (not yours): C/A
Increased Risk for Inflammatory Bowel and Graves Diseases
Elevated susceptibility to inflammatory bowel diseases and Graves' disease is linked to this genetic profile. It represents a 1.5-fold increased risk for Crohn's and a 2-fold increased risk for Graves' disease.
What this genotype means: Increased risk for Crohn's disease and ulcerative colitis; Elevated risk for Graves' disease; Higher susceptibility to 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 [1]. This receptor plays a critical role in the survival and expansion of Th17 cells, which are essential for mucosal immunity and defense against pathogens [1]. However, dysregulated IL-23 signaling can lead to chronic, unchecked inflammation in various tissues [2]. Consequently, genetic variations in IL23R are heavily implicated in susceptibility to several autoimmune and inflammatory disorders [2]. These include inflammatory bowel diseases, psoriasis, and ankylosing spondylitis [3].
Variant Impact: The rs10889677 variant is located in the 3' untranslated region of the IL23R gene, where it directly alters a microRNA binding site [1]. The C to A change disrupts the binding capacity for the regulatory microRNAs let-7e and let-7f [1]. Without these microRNAs to suppress translation, the variant allele leads to enhanced mRNA stability and increased production of the IL-23 receptor protein [1]. This loss of feedback regulation results in sustained pro-inflammatory signaling, contributing to chronic inflammatory diseases [2]. Conversely, the C allele maintains normal microRNA regulation but is independently associated with altered thyroid autoimmune risks [4].
Key Insight: A single letter change in the non-coding region of the IL23R gene prevents microRNAs from turning down receptor production, leading to sustained inflammatory signaling. While the A allele increases the risk of gut and joint inflammation, the C allele paradoxically raises the risk of thyroid-related Graves' disease.
Location: IL23R. Chromosome 1 · 1p31.3 · 67.3 Mb
Estimated prevalence by population
Global 52.6%; European 48.5%; African 70.7%; East Asian 7.6%; South Asian 16.8%; Americas 53.8%; Ashkenazi 43.0%; Finnish 50.0%; Middle Eastern 31.2%; Amish 47.6%.
Estimated CC genotype frequency.
Global 37.9%; European 42.3%; African 26.8%; East Asian 40.0%; South Asian 48.4%; Americas 39.1%; Ashkenazi 45.2%; Finnish 41.4%; Middle Eastern 49.3%; Amish 42.8%.
Estimated CA genotype frequency.
Global 9.5%; European 9.2%; African 2.5%; East Asian 52.4%; South Asian 34.9%; Americas 7.1%; Ashkenazi 11.9%; Finnish 8.6%; Middle Eastern 19.5%; Amish 9.6%.
Estimated AA genotype frequency.
Showing effects for C/C genotype
Immunity & Inflammation
Chronic Inflammatory Diseases
Crohn's Disease. Evidence: 5/10. Source: PMID 17804789. Typical Risk.
Ulcerative Colitis. Evidence: 4/10. Source: PMID 19122664. Typical Risk.
Autoimmune Diseases
Ankylosing Spondylitis. Evidence: 4/10. Source: PMID 21253733. Typical Risk.
Graves' Disease. Evidence: 3/10. Source: PMID 19021011. ~2.3x Increased Risk.
Cancer & Oncology
Colorectal Cancer
Colorectal Cancer. Evidence: 3/10. Source: PMID 31546198. Typical Risk.
Showing effects for A/A genotype
Crohn's Disease. Evidence: 5/10. Source: PMID 17804789. ~1.5x Increased Risk.
Ulcerative Colitis. Evidence: 4/10. Source: PMID 19122664. ~1.5x Increased Risk.
Ankylosing Spondylitis. Evidence: 4/10. Source: PMID 21253733. ~1.3x Increased Risk.
Graves' Disease. Evidence: 3/10. Source: PMID 19021011. Typical Risk.
Colorectal Cancer. Evidence: 3/10. Source: PMID 31546198. Increased Risk.
Showing effects for C/A genotype
Graves' Disease. Evidence: 3/10. Source: PMID 19021011. ~2x Increased Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Presence of two copies of the C allele means the microRNA binding sites in the IL23R gene remain fully intact, allowing normal regulation of receptor expression [1]. This keeps the baseline risk for Crohn's disease and ulcerative colitis at typical population levels [2]. Similarly, the risk for other chronic inflammatory conditions like ankylosing spondylitis remains average [3]. However, this genotype is significantly associated with an elevated susceptibility to Graves' disease, an autoimmune thyroid condition [4]. Research indicates a 2.36-fold overrepresentation of this genotype in patients with Graves' ophthalmopathy [4]. Maintaining a healthy lifestyle and monitoring thyroid function can be beneficial for individuals with this genetic profile.
Typical risk for Crohn's disease and ulcerative colitis; Increased risk for Graves' disease and thyroid-related inflammation.
Sample genotype: AA (Homozygous)
Double copies of the A allele completely disrupt the microRNA binding sites in the IL23R gene, escaping regulation by let-7e and let-7f microRNAs [1]. This leads to enhanced mRNA stability and elevated production of the IL-23 receptor protein, promoting chronic inflammatory responses [1]. As a result, this genotype is associated with a 1.5-fold increased risk for Crohn's disease and ulcerative colitis [2]. It also elevates the risk for ankylosing spondylitis, an inflammatory condition affecting the spine [3]. However, unlike the C allele, the AA genotype is not associated with an increased risk of Graves' disease, remaining at typical baseline levels for thyroid autoimmunity [4]. Supporting gut health and managing chronic inflammation are key considerations for this profile.
Increased risk for Crohn's disease and ulcerative colitis; Higher susceptibility to ankylosing spondylitis; Typical baseline risk for Graves' disease.
Sample genotype: CA (Heterozygous)
A single copy of the A allele disrupts the microRNA binding site in the 3' UTR of the IL23R gene, leading to a loss of regulation by let-7e and let-7f microRNAs [1]. This disruption results in sustained IL-23 receptor expression and increased pro-inflammatory signaling [1]. Consequently, individuals with this genotype have a 1.5-fold higher risk of developing Crohn's disease and ulcerative colitis [2]. There is also an associated increase in susceptibility to ankylosing spondylitis, a chronic inflammatory arthritis [3]. Furthermore, this genotype carries a 2-fold increased risk for Graves' disease, making it a dual risk factor for multiple autoimmune pathways [4]. Managing systemic inflammation through diet and lifestyle may help mitigate these risks.
Increased risk for Crohn's disease and ulcerative colitis; Elevated risk for Graves' disease; Higher susceptibility to ankylosing spondylitis.
Variants with shared genetic architecture
rs11209026 · IL23R Gene · Chr 1 · Autoimmune Disease Risk
rs7517847 · IL23R Gene · Chr 1 · Crohn Disease Risk
rs11465804 · IL23R Gene · Chr 1 · Inflammatory Disease Risk
Association studies of the IL-23R gene in autoimmune thyroid disease in the Japanese population.
Content updated August 2026.
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