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Objective  To determine whether copy number variations (CNVs) in  FCGR3A  and  FCGR3B  are associated with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) in Taiwanese individuals.    Methods   FCGR3A  and  FCGR3B  CNV genotypes were determined in 846 patients with SLE, 948 patients with RA, and 1,420 healthy control subjects, using custom TaqMan CNV assays. The  FCGR3A  and  FCGR3B  CNV genotypes were compared between healthy control subjects and patients and among patients stratified according to clinical characteristics.    Results  A low (<2)  FCGR3A  copy number was significantly associated with SLE (for <2 copies versus 2 copies,  P  = 5.06 × 10 −4 , false discovery rate–corrected  P  [ P  FDR ] = 0.001, odds ratio [OR] 3.26, 95% confidence interval [95% CI] 1.68−6.35) and RA (for <2 copies versus 2 copies,  P  = 5.83 × 10 −4 ,  P  FDR  = 0.0012, OR 2.82, 95% CI 1.56−5.1). A low  FCGR3B  copy number was also significantly associated with SLE (for <2 copies versus 2 copies,  P  = 0.0032,  P  FDR  = 0.0032, OR 1.59, 95% CI 1.17−2.18). Notably, a high (>2)  FCGR3A  copy number was also associated with SLE (for >2 copies versus 2 copies,  P  = 0.003,  P  FDR  = 0.0061, OR 1.6, 95% CI 1.17−2.18). Additionally, the  FCGR3A  low copy number genotype was significantly enriched in subsets of patients with SLE (those with ulcer, arthritis, rash, discoid rash, photosensitivity, nephritis, leukopenia, thrombocytopenia, depressed complement levels, and autoantibody positivity) and patients with RA (those positive for rheumatoid factor) compared with healthy control subjects. The  FCGR3B  low copy number genotype was also significantly enriched in SLE patients with ulcer, rash, discoid rash, photosensitivity, ascites, nephritis, complement level depression, and anti–double‐stranded DNA antibody positivity compared with control subjects. However,  FCGR3B  CNVs were not associated with RA susceptibility (for <2 copy numbers versus 2 copy numbers,  P  = 0.3584, OR 1.15, 95% CI 0.85–1.55) and clinical characteristics.    Conclusion  In Taiwanese individuals, a low  FCGR3A  copy number is a common risk factor for SLE and RA, while a low  FCGR3B  copy number confers a risk of SLE but not RA.

Association of FCGR3A and FCGR3B Copy Number Variations With Systemic Lupus Erythematosus and Rheumatoid Arthritis in Taiwanese Patients