Journal
NATURE GENETICS
Volume 37, Issue 5, Pages 478-485Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ng1540
Keywords
-
Categories
Funding
- NCRR NIH HHS [P20 RR020143] Funding Source: Medline
- NIAID NIH HHS [R01 AI024717] Funding Source: Medline
- NIAMS NIH HHS [P01 AR049084, R01 AR042460] Funding Source: Medline
- NIDCR NIH HHS [R01 DE015223] Funding Source: Medline
Ask authors/readers for more resources
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-kappa B 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available