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Can This Gene Cause Celiac Disease? (ETS1)
The ETS1 gene encodes a protein that turns ‘on’ and ‘off’ multiple genes, including those involved in the development of immune cells. Variants of this gene have been associated with celiac disease and other immune conditions. Read on to learn where your ETS1 variant stands.
What Is the ETS1 Gene?
The ETS1 gene encodes a protein also called ETS1, which is short for ‘E26 transformation-specific sequence 1’. Just as the other 27 members of the ETS family, ETS1 binds to DNA to turn ‘on’ and ‘off’ the expression of multiple genes [R].
ETS1 is mainly expressed in the bone marrow and thymus, as well as in immune cells produced by these tissues such as T cells, B cells, NK cells, and NKT cells. ETS1 promotes the development and activity of the following cell types, while reducing their death [R, R, R, R]:
In contrast, it prevents the development of Th17 and B cells [R, R, R].
ETS1 is also involved in the production of different cytokines and chemokines by these and other cell types, as well as in the activation of cytokine-related pathways [R].
The ETS1 gene encodes a protein that turns ‘on’ and ‘off’ the expression of different genes. ETS1 plays a key role in the immune system by controlling the development, function, and survival of immune cells.
What Is Celiac Disease?
Celiac disease is an immune disorder triggered in response to gluten, a protein found in grains such as wheat, barley, and rye. The immune cells recognize gluten as a threat and mount an aggressive inflammatory response that damages the small intestine and causes digestive issues and nutrient deficiencies due to poor absorption [R, R].
More specifically, the activation of CD4+ T cells by gluten causes their development into Th1 cells and the release of inflammatory cytokines such as IFN-γ and IL-21 [R, R, R, R].
Other immune cells such as CD8+ and Th17 cells can also recognize gluten and trigger inflammation in response to this protein [R, R].
The contribution of ETS1 to celiac disease may be due to its role in the development of any of these cell types.
Celiac disease is a disorder in which the immune system causes inflammation and damages the small intestine in response to gluten, a protein found in most grains. ETS1 may be involved in celiac disease through its role in the development of Th1, CD8+, and Th17 cells.
ETS1 Variants and Immune Conditions
The only ETS1 polymorphism associated with celiac disease is rs11221332. A computer program predicted that the ‘T’ variant may alter the protein production process, and possibly ETS1 levels and activity [R].
In a European study on British, Finnish, Dutch, and Italian populations, the minor allele was one of the variants associated with celiac disease [R].
In contrast, this variant protected against rheumatoid arthritis in a Greek study. Because a more recent Chinese study failed to replicate this result, the authors concluded that ethnic differences may play a key role in this association [R, R].
The ‘T’ variant didn’t increase susceptibility to an autoimmune disease of the liver (primary biliary cirrhosis) in a Chinese study, but carriers had two blood markers of this condition (high total protein and HDL-cholesterol levels) [R].
Illustrating the role of the ETS1 gene in immune function, other polymorphisms have been associated with the following conditions:
- Lupus (rs1128334, rs6590330, rs10893872, and rs7932088) [R, R, R]
- Rheumatoid arthritis (rs73013527) [R]
- Ankylosing spondylitis (rs1128334) [R]
- Primary biliary cirrhosis (rs4937333) [R]
- Psoriasis (rs3802826) [R]
An ETS1 variant that possibly reduces the levels of the protein has been associated with an increased risk of celiac disease. The ETS1 gene is also involved in other immune diseases.
Your ETS1 Results for Celiac Disease
SNP Summary and Table
Primary SNP: ETS1 rs11221332
- ‘C’ = Normal risk of celiac disease.
- ‘T’ = Increased risk of celiac disease.
Population Frequency
The ‘C’ allele is clearly more abundant and 73% of the world population carries two copies versus only 3% of non-carriers.
The ‘T’ allele is even less common in African and East Asian descendants (less than 1% of ‘TT’ in both cases). In contrast, this variant is more abundant in people with European and American ancestry (~40% of carriers).
SNP Table
| variant | genotype | frequency | risk allele |
| rs11221332 |
Recommendations
Diet
Gluten-free Diet
The only effective treatment for celiac disease is a strict gluten-free diet, which allows the management of the symptoms in most cases. Gluten is found in the following grains and their products [R]:
- Wheat
- Rye
- Spelt
- Barley
- Triticale
As previously described, ETS1 plays a role in the development of all types of T cells believed to be involved in celiac disease (Th1, CD8+, and Th17). Variants with increased ETS1 activity may worsen celiac disease by promoting the development of these cells [R, R, R].
Avoiding Lectins/Other Potential Irritants
Dietary lectins may worsen inflammation in people sensitive to them. For example, lectins contributed to autoimmunity in one study with rheumatoid arthritis patients [R, R].
Preliminary research suggests that avoiding lectins may reduce the symptoms of autoimmune conditions in sensitive individuals [R].
Lectins stimulate the production of several pro-inflammatory cytokines, including IFN-γ (whose production by Th1 cells is stimulated by ETS1). Still, more research is needed to clarify the possible connection between lectins and celiac disease [R, R].
Gut damage and inflammation in celiac disease may cause temporary lactose intolerance. Such patients may need to avoid dairy until their gut lining recovers [R].
A cell-based study found that lactose prevents Tregs from inhibiting Th1 and Th17 responses, possibly increasing inflammation. Given the role of ETS1 in promoting Treg development, underactive variants may cause even more inflammation in response to lactose [R, R].
Elimination diets such as the Lectin Avoidance Diet may help identify and remove common food irritants — such as lectins, gluten, and dairy — that may be worsening autoimmunity in sensitive individuals [R, R, R].
The most effective way to treat celiac disease is to go gluten-free. Other potential irritants such as lectins and lactose may worsen autoimmunity in some people.
Lifestyle
Moderate Sun Exposure
Moderate sun exposure is the best way to get natural UV light and vitamin D, which both help suppress inflammation [R, R].
Vitamin D may help overcome the negative effects of overactive ETS1 variants on celiac disease by inhibiting the development of Th1 cells [R, R].
Vitamin D deficiency and subsequent bone issues are common in celiac disease patients, so it’s crucial to get enough of this nutrient [R, R].
A study in mice associated high ETS1 expression with lower blood vitamin D levels, possibly because it activates the enzyme that breaks this vitamin down. People with celiac disease and overactive variants are thus at increased risk of vitamin D deficiency [R, R].
People with celiac disease may have vitamin D deficiency. A moderate exposure to sunlight is a good way to produce this vitamin and reduce inflammation.
Supplements
Black Cumin
Black cumin, also known as black seed, has well-known anti-inflammatory properties.
In one clinical trial, adding 900 mg of black seed oil daily to a gluten-free diet helped restore iron levels and reduce inflammation and gut damage. The same group of authors found that black cumin oil may help with dermatitis herpetiformis, a skin condition caused by celiac disease [R, R].
Preliminary research in animals and cells suggests that black cumin and its active compound thymoquinone may reduce Th1 dominance and IFN-γ release, both of which are associated with celiac disease and ETS1 activity [R, R, R].
Preliminary research suggests that black seed oil may help people with celiac disease reduce gut inflammation and damage.
Disclaimer
The information on this website has not been evaluated by the Food & Drug Administration or any other official medical body. This information is presented for educational purposes only, and may not be used to diagnose or treat any illness or disease.
Also keep in mind that the “Risk Score” presented in this post is based only on a select number of SNPs, and therefore only represents a small portion of your total risk as an individual. Furthermore, these analyses are based primarily on associational studies, which do not necessarily imply causation. Finally, many other (non-genetic) factors can also play a significant role in the development of a disease or health condition — therefore, carrying any of the risk-associated genotypes discussed in this post does not necessarily mean you are at increased risk of developing a major health condition.
Always consult your doctor before acting on any information or recommendations discussed in this post — especially if you are pregnant, nursing, taking medication, or have been officially diagnosed with a medical condition.
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