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Rheumatoid arthritis is an autoimmune disease with a complex etiology, leading to inflammation of synovial tissue and joint destruction. Through a genome-wide association study (GWAS) and two replication studies in the Japanese population (7,907 cases and 35,362 controls), we identified two gene loci associated with rheumatoid arthritis susceptibility ( NFKBIE  at 6p21.1, rs2233434, odds ratio (OR) = 1.20,  P  = 1.3×10 −15 ;  RTKN2  at 10q21.2, rs3125734, OR = 1.20,  P  = 4.6×10 −9 ). In addition to two functional non-synonymous SNPs in  NFKBIE , we identified candidate causal SNPs with regulatory potential in  NFKBIE  and  RTKN2  gene regions by integrating  in silico  analysis using public genome databases and subsequent  in vitro  analysis. Both of these genes are known to regulate the NF-κB pathway, and the risk alleles of the genes were implicated in the enhancement of NF-κB activity in our analyses. These results suggest that the NF-κB pathway plays a role in pathogenesis and would be a rational target for treatment of rheumatoid arthritis.

Functional Variants in NFKBIE and RTKN2 Involved in Activation of the NF-κB Pathway Are Associated with Rheumatoid Arthritis in Japanese