Aim: Some studies have been performed to elucidate the association between Fc gamma receptor 3B (FCGR3B) copy number (CN) and the risk of systemic lupus erythematosus (SLE) and/or lupus nephritis (LN), yet the results remain conflicting. Therefore, we have undertaken a systematic review of all the studies published and carried out a meta-analysis to obtain a better understanding of the role of FCGR3B CN in the susceptibility of SLE and LN.
Method: A computerized literature search was conducted in databases of PubMed, ISI Web of Knowledge for all studies investigating the association between FCGR3B CN and SLE and/or LN, published up to May 2013.
Results: A total of six articles meeting all of the criteria were included in this study. There were five comparisons of SLE between 2490 patients and 4286 controls, and four comparisons of LN between 689 patients and 1924 controls. Our results showed that individuals with FCGR3B CN gain did not suffer an increased risk of SLE or LN as compared to the normal genotype in the total analysis (SLE: OR = 1.07, 95% CI = 0.79-1.45, P = 0.65; LN: OR = 0.83, 95% CI = 0.47-1.46, P = 0.52). However, individuals with FCGR3B CN loss exhibited an increased risk of SLE or LN (SLE: OR = 1.77, 95% CI = 1.51-2.06, P < 0.00001; LN: OR = 2.02, 95% CI = 1.59-2.57, P < 0.00001).
Conclusion: Our meta-analysis indicated that FCGR3B CN loss rather than CN gain was associated with susceptibility to SLE and LN.
Keywords: Fc gamma receptor 3B; copy number variations; lupus nephritis; systemic lupus erythematosus.
© 2014 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd.