TRAF1–C5 as a Risk Locus for Rheumatoid Arthritis — A Genomewide Study

A genomewide association study of North American and Swedish patients with rheumatoid arthritis who were seropositive for autoantibodies against cyclic citrullinated peptide yielded susceptibility variants in the usual suspects: HLA-DRB1 and PTPN22 . A new locus was also implicated: a SNP that lies between the TRAF1 and C5 genes. A genomewide association study of North Americans and Swedes with rheumatoid arthritis yielded susceptibility variants in the usual suspects: HLA-DRB1 and PTPN22 . A new locus was also implicated: a SNP that lies between the TRAF1 and C5 genes. Rheumatoid arthritis is a common inflammatory arthritis of unknown cause, in which both genetic and environmental risk factors have been implicated. 1 – 3 The genetic contribution to a susceptibility to rheumatoid arthritis has been shown in studies of twins 4 and families 5 and in genomewide linkage scans. 6 – 11 Two genes have shown a strong association with susceptibility: PTPN22 12 , 13 and HLA-DRB1 . 14 Variants of each gene elevate the risk primarily for a subgroup of severe rheumatoid arthritis characterized by the presence of autoantibodies against cyclic citrullinated peptide (anti–CCP-positive). 12 , 15 , 16 We have recently reported a significant association at STAT4 on chromosome 2q. . . .