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Kochi, Y. et al.

A functional variant in FCRL3, encoding Fc receptor-like 3, is associated with rheumatoid arthritis and several autoimmunities.

Rheumatoid arthritis is a common autoimmune disease with a complex genetic etiology. Here we identify a SNP in the promoter region of FCRL3, a member of the Fc receptor-like family, that is associated with susceptibility to rheumatoid arthritis (odds ratio = 2.15, P = 0.00000085). This polymorphism alters the binding affinity of nuclear factor-kappaB and regulates FCRL3 expression. We observed high FCRL3 expression on B cells and augmented autoantibody production in individuals with the disease-susceptible genotype. We also found associations between the SNP and susceptibility to autoimmune thyroid disease and systemic lupus erythematosus. FCRL3 may therefore have a pivotal role in autoimmunity.[1]

References

A functional variant in FCRL3, encoding Fc receptor-like 3, is associated with rheumatoid arthritis and several autoimmunities. Kochi, Y., Yamada, R., Suzuki, A., Harley, J.B., Shirasawa, S., Sawada, T., Bae, S.C., Tokuhiro, S., Chang, X., Sekine, A., Takahashi, A., Tsunoda, T., Ohnishi, Y., Kaufman, K.M., Kang, C.P., Kang, C., Otsubo, S., Yumura, W., Mimori, A., Koike, T., Nakamura, Y., Sasazuki, T., Yamamoto, K. Nat. Genet. (2005) [Pubmed]

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