Department of Biochemistry, University of Otago, Box 56, Dunedin, New Zealand.
Hum Mol Genet. 2012 May 15;21(10):2370-6. doi: 10.1093/hmg/dds039. Epub 2012 Feb 14.
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.
尽管低亲和力 IgG 受体基因 FCGR3B 的缺失反复被牵连到系统性自身免疫疾病中，但 FCGR3B 拷贝数变异（CNV）在自身免疫中的作用仍不清楚。研究规模、种族、特定疾病表型和实验方法等因素可能解释了这些相互矛盾的结果。在这里，我们旨在使用荟萃分析来评估 FCGR3B CNV 在自身免疫中的作用。我们排除了使用 SybrGreen 为基础的基因分型的研究，并发现低（<2）FCGR3B CN 与系统性红斑狼疮之间存在强烈的关联[OR=1.59（1.32-1.92），P（荟萃）=9.1×10(-7)]，但与类风湿关节炎无关[OR=1.36（0.89-2.06），P=0.15]。然而，联合自身免疫表型分析支持 FCGR3B 的缺失是无器官特异性自身免疫的风险因素[OR=1.44（1.28-1.62），P（荟萃）=2.9×10(-9)]。这项荟萃分析暗示了清除免疫复合物在非器官特异性自身免疫疾病的发病机制中的作用。
