What you carry at this position in your DNA and what research says about it.
Asthma and Inflammation Risk: 8/10 evidence, 28 publications.
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Sample genotype (not yours): C/C
Lower Asthma Risk but Higher CRP
With intact classic IL-6 signaling, this genotype has higher C-reactive protein and fibrinogen, but lower soluble IL-6 receptor and a reduced risk of developing asthma.
What this genotype means: Higher baseline C-reactive protein levels; Reduced genetic risk for asthma; Slightly higher risk for ankylosing spondylitis.
Sample genotype (not yours): C/T
Typical Asthma and Inflammatory Risk Profile
Carrying one copy of each allele results in intermediate levels of inflammatory markers. This leads to a typical, balanced risk profile for both respiratory and autoimmune conditions.
What this genotype means: Typical baseline inflammatory marker levels; Average genetic risk for asthma; Balanced risk for autoimmune joint conditions.
Sample genotype (not yours): T/T
Higher Asthma Risk but Lower CRP and Fibrinogen
This genotype sheds more soluble IL-6 receptor, raising asthma risk via IL-6 trans-signaling; but because classic signaling is impaired, C-reactive protein and fibrinogen are actually lower (the same effect as the drug tocilizumab).
What this genotype means: Lower baseline C-reactive protein levels; Increased genetic risk for asthma; Reduced risk of ankylosing spondylitis.
Gene function and biological role
Gene Function: The IL6R gene encodes the receptor for interleukin-6, a vital signaling protein that coordinates the body's inflammatory response to injury and infection [1]. When interleukin-6 binds to this receptor, it triggers a cascade that promotes antibody production and prompts the liver to synthesize C-reactive protein [1] [2]. This receptor exists in both a cell-bound form and a soluble form that circulates freely in the blood [3]. Elevated levels of the soluble receptor can amplify systemic inflammation by enabling interleukin-6 to activate cells that normally lack the receptor [3]. Consequently, genetic variations in this gene are major determinants of susceptibility to chronic inflammatory and autoimmune diseases [4].
Variant Impact: The rs4129267 variant is an intronic change in the IL6R gene that is in near-perfect linkage disequilibrium with a functional coding variant [3]. This close genetic link means rs4129267 serves as a highly reliable proxy for receptor shedding, a process where the interleukin-6 receptor is clipped from cell membranes and released into circulation [3]. The T allele of this variant significantly increases the levels of this soluble receptor, leading to higher baseline systemic inflammation [1]. Conversely, this same genetic change alters the risk profile for various autoimmune diseases, creating a complex biological trade-off [4]. It represents one of the most well-studied examples of how a single genetic locus can balance susceptibility between different types of inflammatory disorders [5].
Key Insight: This variant acts as a genetic see-saw, where the same allele that increases your risk for asthma and systemic inflammation actually lowers your risk for joint-fusing ankylosing spondylitis.
Location: IL6R. Chromosome 1 · 1q21.3 · 154.5 Mb
Origin Story: Parasites and infectious pathogens have historically acted as major evolutionary pressures on interleukin genes, shaping the distribution of these inflammatory variants across different global populations.
Estimated prevalence by population
Global 47.6%; European 36.8%; African 74.4%; East Asian 41.0%; South Asian 50.4%; Americas 26.2%; Ashkenazi 34.7%; Finnish 52.1%; Middle Eastern 38.3%; Amish 27.8%.
Estimated CC genotype frequency.
Global 40.6%; European 47.7%; African 23.7%; East Asian 46.0%; South Asian 41.2%; Americas 50.0%; Ashkenazi 48.4%; Finnish 40.1%; Middle Eastern 47.2%; Amish 49.8%.
Estimated CT genotype frequency.
Global 11.8%; European 15.4%; African 1.9%; East Asian 12.9%; South Asian 8.4%; Americas 23.9%; Ashkenazi 16.9%; Finnish 7.7%; Middle Eastern 14.5%; Amish 22.3%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Organ Systems
Respiratory Health
Asthma. Evidence: 8/10. Source: PMID 21907864. Typical Risk.
Immunity & Inflammation
Inflammatory & Circulating Protein Markers
C-Reactive Protein. Evidence: 10/10. Source: PMID 22579472. Higher Levels.
Autoimmune Diseases
Ankylosing Spondylitis. Evidence: 6/10. Source: PMID 23749187. Increased Risk.
Cardiovascular & Metabolic
Coagulation & Clotting
Fibrinogen Levels. Evidence: 8/10. Source: PMID 23969696. Elevated Levels.
Showing effects for C/T genotype
Asthma. Evidence: 8/10. Source: PMID 21907864. Slightly Increased.
C-Reactive Protein. Evidence: 10/10. Source: PMID 22579472. Typical Levels.
Ankylosing Spondylitis. Evidence: 6/10. Source: PMID 23749187. Typical Risk.
Fibrinogen Levels. Evidence: 8/10. Source: PMID 23969696. Typical Levels.
Showing effects for T/T genotype
Asthma. Evidence: 8/10. Source: PMID 21907864. ~1.1x Higher Risk.
C-Reactive Protein. Evidence: 10/10. Source: PMID 22579472. Lower Levels.
Ankylosing Spondylitis. Evidence: 6/10. Source: PMID 23749187. Reduced Risk.
Fibrinogen Levels. Evidence: 8/10. Source: PMID 23969696. Lower Levels.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Inheriting two copies of the C allele is associated with lower levels of soluble interleukin-6 receptors, but higher C-reactive protein and fibrinogen [1]. Because less receptor is shed for IL-6 trans-signaling, this genotype is linked to a lower risk of developing asthma and respiratory issues [2]. However, this lower receptor shedding means more receptors remain bound to cell membranes, which can alter immune signaling in other ways [1]. Specifically, this genotype is associated with an increased risk of joint-related autoimmune conditions, such as ankylosing spondylitis [1]. It is also linked to slightly higher levels of fibrinogen, a protein involved in blood clotting [3]. Overall, this genotype represents a baseline state for respiratory health but carries a slightly elevated risk for specific joint and bowel inflammatory conditions [1].
Higher baseline C-reactive protein levels; Reduced genetic risk for asthma; Slightly higher risk for ankylosing spondylitis.
Sample genotype: CT (Heterozygous)
Having the heterozygous C/T genotype means carrying one copy of each allele, resulting in intermediate levels of soluble interleukin-6 receptors and C-reactive protein [1]. This intermediate state balances the genetic risks associated with this locus, providing a typical risk profile for asthma [2]. It also results in a moderate, typical risk for joint-fusing inflammatory conditions like ankylosing spondylitis [1]. Fibrinogen levels and other blood clotting factors generally remain within the normal, typical range [3]. This genotype represents the most common genetic profile in many populations, representing a balanced middle ground in the immune system's inflammatory response.
Typical baseline inflammatory marker levels; Average genetic risk for asthma; Balanced risk for autoimmune joint conditions.
Sample genotype: TT (Homozygous)
Carrying two copies of the T allele is associated with approximately 73% higher levels of soluble interleukin-6 receptors, but LOWER C-reactive protein and fibrinogen, because this receptor-shedding allele impairs classic IL-6 signaling (the same mechanism as the drug tocilizumab) [1]. The higher soluble receptor drives IL-6 trans-signaling, a major driver of airway hyperresponsiveness and is linked to a higher risk of developing asthma [2]. However, because more receptors are shed into the bloodstream, fewer remain on cell surfaces to drive localized tissue damage [1]. As a result, this genotype is highly protective against ankylosing spondylitis, a chronic inflammatory arthritis of the spine [1]. It is also associated with lower levels of fibrinogen and a reduced risk of abdominal aortic aneurysms [3]. While it elevates respiratory and general inflammatory risks, it provides a unique shield against specific chronic autoimmune diseases [1].
Lower baseline C-reactive protein levels; Increased genetic risk for asthma; Reduced risk of ankylosing spondylitis.
Variants with shared genetic architecture
rs2228145 · IL6R Gene · Chr 1 · Inflammation and Allergies
rs12083537 · IL6R Gene · Chr 1 · Systemic Inflammation
rs4537545 · IL6R Gene · Chr 1 · Heart Disease Risk
The IL6R variation Asp(358)Ala is a potential modifier of lung function in subjects with asthma.
Identification of IL6R and chromosome 11q13.5 as risk loci for asthma.
Content updated August 2026.
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