Meta-analysis evidence of a differential risk of the FCRL3 -169T->C polymorphism in white and East Asian rheumatoid arthritis patients

Steven J. Schrodi, Celera, Inc
Begovich Ann, Celera, Inc
Chang Monica, Celera, Inc

Abstract

Association between a functional promoter polymorphism (rs7528684) in the Fc receptor-like gene, FCRL3, and rheumatoid arthritis (RA) has been observed in 3 independent Japanese case-control sample sets ([1][2]). Studies examining the role of this polymorphism in risk of RA in 9 independent white sample sets, however, have yielded conflicting results ([3-8]). Further, a large study of Korean subjects failed to demonstrate association of this single-nucleotide polymorphism (SNP) with RA ([9]). Although the precise function of FCRL3, which has strong structural homology with the classic Fc receptors, is unknown, the existing data are consistent with the hypothesis that it may influence the fate of B cells and augment the emergence of self-reactive cells in the germinal center (for review, see ref.[1]), making it an excellent candidate gene for autoimmune disease. Consequently, we undertook a meta-analysis of the data from these 13 study samples, analyzing East Asians (3,172 cases and 2,916 controls) and whites (5,645 cases and 5,592 controls) separately. Our findings indicate that, although the data support the notion that rs7528684 has a role in risk of RA among East Asians, there is no reliable evidence of an association of this SNP with RA in whites of European descent.