FCGR2C rs10917661: Understanding the Gln13Ter Variant
The rs10917661 variant is a genetic change in the FCGR2C gene that acts as a stop-gain polymorphism, influencing whether the body produces a specific immune receptor. Researchers have investigated this variant for potential associations with autoimmune conditions and allergic responses, though evidence remains limited.
What each genotype means
Functional receptor expression
This genotype corresponds to the FCGR2C-ORF (open reading frame) variant, which allows for the expression of the FcγRIIC receptor protein. Research indicates this receptor is involved in immune activation, though studies have not consistently linked this specific variant to increased risk for asthma or atopy. This is considered the functional form of the gene compared to the non-functional pseudogene variant.
The functional ORF allele is found in approximately 10-15% of individuals of European ancestry.
Mixed receptor expression
This heterozygous genotype indicates the presence of both the functional ORF allele and the non-functional stop-codon allele. Individuals with this profile may have reduced overall expression of the FcγRIIC receptor compared to those with two functional copies. Current evidence does not suggest this genotype significantly alters susceptibility to common allergic conditions.
This heterozygous genotype is observed in a significant portion of the population, consistent with the minor allele frequency of 0.15-0.25 for the stop-codon variant.
Non-functional receptor expression
This genotype represents the FCGR2C-Stop variant, where a stop codon prevents the production of the functional FcγRIIC protein, effectively rendering the gene a pseudogene in these individuals. While this variant is a focus of research regarding immune system regulation, it has not been definitively associated with clinical outcomes like asthma or atopy in major studies. This is the most common state for this gene in many populations.
This is the most common genotype in many populations, as the stop-codon allele is the predominant form of the gene.
What is rs10917661?
The variant rs10917661 is a single nucleotide polymorphism (SNP) located within the FCGR2C gene on chromosome 1. This specific change is often described as a Gln13Ter (glutamine to termination) polymorphism. In genetic terms, a stop-gain or 'nonsense' mutation introduces a premature stop codon in the DNA sequence. This effectively tells the cellular machinery to stop building the protein prematurely. Because of this, the variant determines whether the FCGR2C gene produces a functional protein or remains a non-functional pseudogene. When the protein is produced, it functions as an activating Fc gamma receptor, which is part of the immune system's toolkit for recognizing and responding to antibodies attached to pathogens or other targets.
The Role of the FCGR2C Gene
The FCGR2C gene encodes the Fc gamma receptor IIc (FcγRIIc) protein. This receptor belongs to a family of proteins found on the surface of various immune cells, such as natural killer cells and other white blood cells. These receptors are responsible for binding to the 'tail' (Fc region) of immunoglobulin G (IgG) antibodies. By binding these antibodies, the receptors help the immune system identify and clear immune complexes, participate in phagocytosis, and trigger cellular activation. Because FCGR2C is highly homologous to other receptors like FCGR2B and FCGR2A, its expression can significantly alter the balance of activating and inhibitory signals within the immune system. Whether this receptor is expressed depends heavily on the specific genotype at the rs10917661 position.
Research and Associations
Scientific interest in rs10917661 stems from its potential to modify immune responses. Some studies have explored whether the presence of the functional FCGR2C protein is associated with autoimmune diseases, such as idiopathic thrombocytopenic purpura (ITP) or systemic lupus erythematosus. In the context of allergies and asthma, researchers have investigated whether this variant contributes to disease susceptibility. However, the evidence is currently mixed or limited. For instance, some studies have found no significant association between this specific SNP and asthma or atopy in certain cohorts. Because immune regulation is complex and involves many genes, it is difficult to isolate the effect of a single variant. Consequently, while the variant is biologically functional, its clinical impact as a standalone risk factor for specific diseases remains a subject of ongoing investigation rather than a settled medical fact.
Understanding Your Results
If you have received information about your rs10917661 genotype, it is important to view it within the context of current scientific uncertainty. Genetic associations are statistical observations made across large populations and do not predict individual health outcomes. Many factors, including environment, lifestyle, and other genetic variants, contribute to the development of immune-related conditions. You cannot use this information to diagnose yourself with an allergy or autoimmune disorder, nor should it be used to make decisions about medical treatments. If you have concerns about your immune health or potential allergic reactions, the most appropriate step is to consult with a qualified clinician or an immunologist. They can provide a comprehensive evaluation based on your clinical history and symptoms, which is far more informative than any single genetic variant.
How common is this variant?
The minor allele frequency for rs10917661 is approximately 0.15 to 0.25 in European and American populations, indicating that the variant is relatively common across these groups.
Frequently asked questions
Is rs10917661 a cause of allergies?
Current research has not established rs10917661 as a direct cause of allergies. While some studies have investigated its role in immune responses, the evidence linking this specific variant to asthma or atopy is limited and often shows no significant association.
Does this variant mean I have an immune deficiency?
No. The FCGR2C variant influences the expression of a specific receptor, but it does not equate to a clinical immune deficiency. The human immune system has significant redundancy, and the absence of this specific receptor is not typically associated with overt immunodeficiency.
Can I use this genotype to predict my risk of autoimmune disease?
Genetic variants like rs10917661 are only one small piece of a very complex puzzle. They cannot be used to predict individual risk for autoimmune diseases, as these conditions are influenced by a wide array of genetic and environmental factors.
Should I change my medication based on this SNP?
No. You should never change your medication or treatment plan based on genetic test results without consulting your doctor. Always discuss any concerns about your health or medications with a qualified healthcare professional.
Sources & further reading
Educational information only, last refreshed 9/22/2026. Not medical advice — these associations describe population statistics, not individual predictions.
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