Meta-analysis confirms a role for deletion in FCGR3B in autoimmune phenotypes.

Abstract

Although deletion in the low-affinity IgG receptor gene FCGR3B has repeatedly been implicated in systemic autoimmune disease, the role of FCGR3B copy number variation (CNV) in autoimmunity still remains unclear. Factors such as study size, ethnicity, specific disease phenotype and experimental methodology may explain these conflicting results. Here we aimed at using meta-analysis to assess the role for FCGR3B CNV in autoimmunity. We excluded studies using SybrGreen-based genotyping and found strong evidence for association between low (<2) FCGR3B CN and systemic lupus erythematosus [OR = 1.59 (1.32-1.92), P(meta)=9.1 × 10(-7)], but not for rheumatoid arthritis [OR = 1.36 (0.89-2.06), P= 0.15]. However, a combined autoimmune phenotype analysis supports the deletion of FCGR3B as a risk factor for non-organ-specific autoimmunity [OR = 1.44 (1.28-1.62), P(meta)= 2.9 × 10(-9)]. This meta-analysis implicates the clearance of immune complex in the etiology of non-organ-specific autoimmune disease.

• Authors: Cushla McKinney, Tony R Merriman
• Journal: Human molecular genetics (Hum Mol Genet) Vol. 21 Issue 10 Pg. 2370-6 (May 15 2012) ISSN: 1460-2083 [Electronic] England
• PMID: 22337955 (Publication Type: Journal Article, Meta-Analysis, Research Support, Non-U.S. Gov't)

Chemical References

• FCGR3B protein, human
• GPI-Linked Proteins
• Receptors, IgG

Topics

• Autoimmune Diseases (genetics, metabolism)
• DNA Copy Number Variations
• GPI-Linked Proteins (genetics, metabolism)
• Genetic Predisposition to Disease
• Genotype
• Humans
• Lupus Erythematosus, Systemic (etiology, genetics, immunology)
• Phenotype
• Receptors, IgG (genetics, metabolism)
• Sequence Deletion