A mutation previously shown to predict the risk for rheumatoid arthritis (RA) and other autoimmune diseases in Asian individuals is also involved in the development of the disease in Caucasians, say researchers. "Our findings lend support for this polymorphism in RA across ethnically diverse populations, and, suggestions of involvement in juvenile idiopathic arthritis also warrant follow-up studies," remark Morten Eike (Rikshospitalet, Oslo, Norway) and associates. Eike et al note that recent research has proposed the gene encoding Fc receptor-like 3 (FCRL3) as a novel autoimmune predisposing factor. "A single nucleotide polymorphism (SNP) located in the promoter region (2169T/C) of this gene was reported associated with RA, systemic lupus erythematosus, Graves disease, and Hashimoto thyroiditis in a Japanese population," the researchers write in the Annals of the Rheumatic Diseases. To determine whether mutations in FCRL3 influence the risk for autoimmune disorders in other populations, the investigators genotyped a Scandinavian panel of patients with autoimmune diseases, including 708 with RA, 524 with juvenile idiopathic arthritis, 116 with ulcerative colitis, 365 with primary sclerosing cholangitis, 148 with Crohn's disease. These patients were compared with 1030 generally healthy control volunteers, who were recruited from the blood donor register at Ulleva/l University Hospital, Oslo. This research revealed that RA was associated with the C allele and the CC genotype of the FCRL3 2169T/C polymorphism, giving risk ratios of 1.16 and 1.30, respectively. There was also a statistical suggestion of a link between the risk of juvenile idiopathic arthritis and the CC genotype, with an odds ratio of 1.30. However, FCRL3 mutations had no significant effect on the risk of any other of the auto-immune conditions studied. The authors note that the impact of the FCRL3 2169T/C polymorphism on RA risk was smaller than seen in previous studies conducted in Japanese individuals, which "could explain the conflicting results seen in other studies," they suggest. Discussing the moderate link they found between FCRL3 mutations and juvenile idiopathic arthritis risk, the investigators highlight the need for further large studies in individuals with well-characterized disease. Until such studies are conducted the authors concede that "it is difficult to say whether our results reflect a relationship with adult RA, whether clinical features specific for juvenile idiopathic arthritis are involved, or if ours was a chance finding."
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