NDLI: Association of FCGR3A and FCGR3B copy number variations with systemic lupus erythematosus and rheumatoid arthritis in Taiwanese patients.

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Association of FCGR3A and FCGR3B copy number variations with systemic lupus erythematosus and rheumatoid arthritis in Taiwanese patients.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Chen, Ji-Yih Wang, Chin-Man Chang, Su-Wei Cheng, Ching-Hui Wu, Yeong-Jian Jan Lin, Jing-Chi Yang, Bing Ho, Huei-Huang Wu, Jianming
Spatial Coverage	Taiwan
Description	Country affiliation: China Author Affiliation: Chen JY ( Chang Gung University College of Medicine, Taiwan, Republic of China.)
Abstract	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 [PFDR ] = 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) , PFDR = 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, PFDR = 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, PFDR = 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.
File Format	HTM / HTML
ISSN	23265191
e-ISSN	23265205
DOI	10.1002/art.38813
Journal	Arthritis & Rheumatology
Issue Number	11
Volume Number	66
Language	English
Publisher	Wiley
Publisher Date	2014-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Rheumatology Dna Copy Number Variations Genetics Lupus Erythematosus, Systemic Receptors, Igg Rheumatic Fever Adolescent Case-control Studies Gpi-linked Proteins Genetic Predisposition To Disease Genotype Epidemiology Phenotype Risk Factors Taiwan Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology Rheumatology

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