Human Fc␥ receptor (Fc␥R) genes form a clustered gene family on chromosome 1q21-24. Although the association of Fc␥R polymorphisms with systemic lupus erythematosus (SLE) has been extensively studied, the results are often contradictory. In this study, Fc␥RIIA-131H/R, Fc␥RIIIA-176F/V and Fc␥RIIIB-NA1/2 genotypes were determined in the Japanese patients with SLE (n = 81) or rheumatoid arthritis (RA, n = 115) as well as in healthy individuals (n = 217), and possible association with the disease was tested using case-control analysis. Unlike in other populations, significant difference was not observed in the frequencies of Fc␥RIIA and Fc␥RIIIA genotypes between patients with SLE and healthy individuals. However, significant difference was detected in the frequencies of Fc␥RIIIB genotypes between SLE and healthy individuals (P = 0.008). The odds ratio [OR] of the Fc␥RIIIB-NA2/NA2 homozygotes for the development of SLE was 2.52 (95% confidence interval [CI]: 1.33-4.79). Among the patients with SLE, individuals with NA2/2 were significantly more likely to have lupus nephritis (P = 0.007). No association was observed between any of the Fc␥R polymorphisms and RA. Significant linkage disequilibrium was detected between Fc␥RIIIA and IIIB, but neither between IIA and IIIA, nor between IIA and IIIB. These observations may underscore the relevance of defective immune complex handling in the pathogenesis of SLE, or may suggest the presence of primarily associated gene(s) in linkage disequilibrium with Fc␥R genes.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.