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CD2

T Cells & Tregs in Autoimmunity & Rheumatoid Arthritis (CD2/CD101)

Written by Jasmine Foster, BSc, BEd on November 18th, 2020
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CD2 & CD101 are two closely related genes that regulate T cell and Treg activity. How do they play into rheumatoid arthritis? Find out here.

Summary

CD2 and CD101 encode two white blood cell surface proteins. Variants of CD2 and CD101 may play a role in rheumatoid arthritis by increasing inflammatory T cells and reducing Tregs. Lifestyle, diet, and supplement modifications may counteract the effects of these variants by increasing Tregs and correcting the balance between different types of T cells.

CD2/CD101 and Rheumatoid Arthritis

A variant that may affect the function or expression of either the CD2 or CD101 gene has been associated with increased rates of rheumatoid arthritis [R, R].

CD2 encodes cluster of differentiation 2, a protein found on the surface of some types of white blood cells. CD2 helps T cells develop and move around the body, promoting an immune response. CD101 encodes cluster of differentiation 101, also known as IGSF2 or immunoglobulin superfamily member 2. CD101 is similarly expressed on the surface of some white blood cells, but it is believed to have an anti-inflammatory function [R, R, R].

Both CD2 and CD101 have been implicated in a variety of diseases, which isn’t surprising given their presence on important immune cells. The most significant of these associations is with diabetes and rheumatoid arthritis [R, R, R].

People with rheumatoid arthritis may have a modified version of CD2 on their T cells that increases the intensity of the immune response. Some researchers believe that preventing CD2 from interacting with other immune molecules, especially CD58, may help slow the progression of arthritic disease [R, R].

By contrast, CD101 is believed to increase the activity of Treg cells, which are anti-inflammatory and prevent immune reactions to harmless triggers [R].

CD2 and CD101 are both linked to a variant associated with rheumatoid arthritis. CD2 increases the activity of certain T cells, while CD101 promotes anti-inflammatory Tregs.

Your CD2/CD101 Results for Rheumatoid Arthritis

SNP Table

variant genotype frequency risk allele
rs624988

 

CD2/CD101 rs624988 [R, R]

  • ‘C’ = Not associated with rheumatoid arthritis
  • ‘T’ = Associated with relatively increased rates of rheumatoid arthritis
  • The ‘T’ allele may alter the activity of both pro- and anti-inflammatory T cells [R, R].

 

Recommendations

CBD Oil

In a laboratory setting, exposure to CBD oil activates anti-inflammatory Tregs. These Tregs became active even under circumstances that would otherwise suppress their anti-inflammatory action, which would be especially helpful in people with high CD2 and low CD101 [R, R].

In a small study of 58 rheumatoid arthritis patients, a cannabis extract containing both CBD and THC significantly reduced pain and quality of sleep. Some research suggests that the combination of CBD and THC is more effective than CBD alone; however, CBD oil is much more readily available and considered non-psychoactive [R].

In mice with this condition, oral and injected CBD relieved inflammation and slowed the joint damage progression. CBD also prevented T cells and joint cells (synoviocytes) from reproducing and releasing pro-inflammatory cytokines (TNF-alpha and IFN-gamma) [R].

Similarly, a topical CBD gel reduced joint swelling, pain, and the levels of inflammatory markers (such as TNF-alpha) in the nerves of rats with rheumatoid arthritis [R].

Additionally, synthetic CBD-like compounds reduced inflammation, pain perception, and joint damage in mice and rats with this type of arthritis [R, R, R].

Two studies in humans and dogs found that animals with rheumatoid arthritis or osteoarthritis had higher levels of both CB receptors and several cannabinoids in the joints. This suggests that the body activates the endocannabinoid system to fight arthritis. In line with this, increasing cannabinoids may be a good therapeutic strategy [R, R].

CBD oil may correct the downstream effects of dysfunctional CD2 and CD101. It has also shown promise as a supplement in rheumatoid arthritis patients.

Omega-3 Fatty Acids

Omega-3s, and especially DHA, increase Treg levels in cell and mouse studies. This may be helpful for people with low or dysfunctional CD101 [R, R, R].

Studies suggest that increased dietary intake of omega-3 fatty acids may protect against rheumatoid arthritis. In a meta-analysis of 20 clinical trials, higher omega-3 consumption improved rheumatoid arthritis symptoms and lab markers [R, R].

Good dietary omega-3 sources include [R]:

Omega-3 fatty acids such as those found in fish, seeds, and nuts may help protect against rheumatoid arthritis by increasing Tregs.

Fish Oil

Fish oil is the richest source of DHA, an omega-3 fatty acid that increases Tregs [R, R, R].

Supplementation with fish oil may lower the activity of chronic inflammatory and autoimmune diseases, including rheumatoid arthritis [R, R].

A meta-analysis of 17 trials found that supplemental fish oil reduced inflammatory joint pain from rheumatoid arthritis and other inflammatory conditions [R].

In one study of 250 patients, omega-3’s were as effective as ibuprofen in reducing pain caused by arthritis [R].

Resolvins found in EPA and DHA appear to prevent certain inflammatory cytokines such as TNF-α from inducing pain [R].

Fish oil is the richest source of DHA, an omega-3 fatty acid that increases Tregs and may help improve the symptoms of rheumatoid arthritis.

Lactobacillus casei Probiotics

In mice, Lactobacillus casei probiotics significantly increased Tregs and reduced cytokines in the blood [R].

In 2 clinical trials on over 100 people with rheumatoid arthritis, supplementation with a Lactobacillus casei strain for 8 weeks reduced joint pain and inflammation [R, R].

This strain also relieved rheumatoid arthritis in mice and rats [R, R, R].

casei probiotics may improve rheumatoid arthritis symptoms by increasing Tregs.

Author photo
Jasmine Foster
BSc, BEd

Jasmine received her BS from McGill University and her BEd from Vancouver Island University.

Jasmine loves helping people understand their brains and bodies, a passion that grew out of her dual background in biology and education. From the chem lab to the classroom, everyone has the right to learn and make informed decisions about their health.

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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