FCRL3

SNP Table

variant	genotype	frequency	risk allele
rs7522061
rs56273037
rs57500528
rs2026391
rs2252176
rs12140725
rs14335
rs11264798
rs2210912
rs2210913
rs3761959
rs6681271
rs945635
rs1571872
rs1885561
rs2758696
rs2758697
rs2282284
rs4284256
rs11264794

23572 associated SNPs in total

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Summary Blog Articles GHR Function Frequently Asked Questions

Summary

FCRL3 encodes Fc receptor-like 3, a protein that may promote inflammation by inhibiting the functions of regulatory immune cells. Variants of FCLR3 may play a role in rheumatoid arthritis by increasing production or activity of Fc receptor-like 3. They may also be linked to thyroid autoimmunity. Mutations in this gene are associated with rheumatoid arthritis, thyroid diseases, and lupus (R).

Lifestyle and supplement modifications may counteract the effects of these variants by suppressing a protein required to induce Fc receptor-like 3 production, and by activating regulatory immune cells.

Protein names

Fc receptor like 3 [Source:HGNC Symbol;Acc:HGNC:18506]

Found in These Blog Articles

The Missing Link Between Immunity and Thyroid Disorders (FCRL3)

FCRL3 has complex roles in immune system regulation. Click to learn about its variants associated with thyroid autoimmunity.

Regulatory Immune Cells & Rheumatoid Arthritis Development (FCRL3)

FCRL3 may promote inflammation. Variants of FCRL3 have been associated with rheumatoid arthritis. Read more here.

GHR Function

More Information

FCRL3 (Fc receptor-like 3) gene encodes for a receptor with complex roles in the immune system. It can send both inhibitory and stimulatory signals to immune cells upon activation, enabling it to modulate the body’s response to infectious agents and other threats [R, R].

As its full name suggests, FCRL3 resembles Fc receptors on immunoglobulin (antibody) chains. Despite recent progress in understanding, scientists are still exploring its exact roles in immunity [R, R].

Both B-cells and T-cells express FCRL3 receptors, which mediate their communication and development. Unfortunately, like many other genes involved in immune response, FCRL3 has a dark side—certain variations may impair its function and correlate with autoimmunity [R, R].

The FCRL3 gene codes for Fc receptor-like 3, a receptor that can stimulate or inhibit certain functions of immune system cells upon its activation [R, R].

Fc receptor-like 3 is found on the surfaces of different types of immune cells, such as regulatory T cells (Tregs). Its production can be exacerbated by the inflammatory protein NF-kB [R, R].

Tregs are involved in suppressing the formation of autoantibodies, or antibodies that recognize the body’s own tissues. In this manner, Tregs may function to prevent rheumatoid arthritis and other autoimmune disorders [R, R, R].

Back in 2005, a group of Japanese authors investigated the connection between the SNPs in FCRL3 and different autoimmune conditions. According to their results, the "G" allele at rs7528684 correlates with thyroid autoimmunity—particularly Graves' disease [R].

The study provided valuable insights into the mechanisms behind FCRL3-associated autoimmunity, which we’ll discuss later.

A clinical trial of nearly 2,000 UK subjects confirmed the link between rs7528684-G and Graves’ disease (GD) in Europeans. Carriers of this allele had 17% higher GD rates. Another FCRL3 variant, rs3761959-T, showed an even stronger association and correlated with 20% higher disease rates [R].

In 2,500 people of European ancestry, scientists identified another SNP associated with Graves’ disease: people with the “C” allele at rs7522061 had 25% higher GD incidence. According to the study, rs7522061 is a “twin” SNP of rs3761959 rather than a separate factor [R].

Two Chinese studies of 20,000 total participants came to similar conclusions for two primary SNPs: rs3761959-T and rs7528684-G correlated with 22-23% higher rates of Graves' disease [R, R].

The above variations also correlated with Graves' ophthalmopathy (GO), a complication that attacks the eyes, in another Chinese study of 1,200 people [R].

In different populations across the globe, they’ve been associated with other autoimmune conditions, such as [R, R, R]:

Rheumatoid arthritis
Lupus
Type 1 diabetes
Multiple sclerosis

However, it’s important to note that the risk/beneficial alleles are not the same for each disease. In other words, those with a specific FCRL3 variant can be prone to one condition but protected against another.

In rheumatoid arthritis, autoantibodies specific for joints attract components of the immune system to these regions. This can result in joint inflammation and joint thickening, leading to symptoms such as pain [R].

Recent studies have suggested that Fc receptor-like 3 may have an inhibitory effect on Tregs. In line with this, a greater amount of Fc receptor-like 3 on the surfaces of Tregs has been linked to rheumatoid arthritis progression [R].

Indeed, variants of FCRL3 have been associated with rheumatoid arthritis. Similar to the effects of NF-kB, these variants may increase production or activity of Fc receptor-like 3, leading to suppression of Treg function, increased formation of antibodies specific for joints, and inflammation [R, R].

Frequently Asked Questions

Why Are Alleles for This SNP Different Elsewhere? Major vs. Reference Allele Is My Variant Good or Bad? SNP vs. Mutation

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