中华皮肤科杂志 ›› 2002, Vol. 35 ›› Issue (4): 260-262.

• 论著 • 上一篇    下一篇

湖南汉族系统性红斑狼疮患者FcγRⅢa—158V/F多态性研究

谢红付, 朱蓉, 施为, 杜乾君, 陈明亮   

  1. 中南大学湘雅医院皮肤科 长沙 410078
  • 收稿日期:2001-07-24 出版日期:2002-08-15 发布日期:2002-08-15

Polymorphism of Fc Gamma Receptor TypeⅢ in Han Patients with Systemic Lupus Erythematosus from Hunan Province

XIE Hongfu, ZHU Rong, SHI Wei, DU Qianjun, CHEN Mingliang   

  1. Department of Dermatology, Xiang Ya Hospital of Central South University, Hunan 410078, China
  • Received:2001-07-24 Online:2002-08-15 Published:2002-08-15

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摘要： 目的 探讨中国湖南汉族SLE患者与FcγRⅢa-158V/F多态性的相关性.方法 SLE患者65例,其中狼疮肾炎患者38例,采用多聚酶链反应(PCR)和限制性片段长度多态性分析法(RFLP)检测FcγRⅢa-158V/F基因型,并与60例正常人进行比较.结果 ①与对照组相比,SLE患者FcγRⅢa-158F/F纯合子基因型显着增高(OR=2.23,χ2=4.69,P=0.03).②与对照组相比,狼疮肾炎患者Fc-γRⅢa-158F/F纯合子基因型和FcγRⅢa-158F等位基因频率均显着增高(OR=2.67,χ2=5.36,P=0.02;OR=2.00,χ2=4.91,P=0.03).结论 SLE患者FcγRⅢa-158F/F纯合子基因型显着增高,狼疮肾炎患者FcγRⅢa-158F/F纯合子基因型和FcγRⅢa-158F等位基因频率均显着增高,提示FcγRⅢa多态性与SLE相关,FcγRⅢa-158F等位基因可能是狼疮肾炎的危险因素.

关键词: 红斑狼疮,系统性, 受体,IGG, 免疫球蛋白同种异型

Abstract: Objective To investigate the association betw een systemic lupus erythematosus(SLE)and polymorphismof Fc gamma receptor ty peⅢin Han patients fromHunan province.Methods Genotypes of FcγRⅢa-158V/F were determined by polymerase chain reaction(PCR)and restriction fragment length polymorphism(RFLP)analysis in 65 patients with SLE and 60normal controls.Results ①It was found that the frequency of homozygous FcγRⅢa-158F/F genotype was significantly h igher in patients with SLE than that i n controls(OR=2.23,χ2=4.69,P=0.03).②The frequencies of both homozygous FcγRⅢa-158F/F genotype and FcγRⅢa-158F allele were significantly high er in patients with lupus nephritisc ompared with those in controls(OR=2.67,χ2=5.36,P=0.02;OR=2.00,χ2=4.91,P=0.03).Conclusions These results suggest that an abnorm al distribution of FcγRⅢa-158V/F polymorphism is associated with SLE in the Hans of Hunan province,and the presence of FcγRⅢa-158F allele is a risk factor for lupus nephritis.These findings support the hypothesis of a genetic mechanism in the pathogenesis of SLE.

Key words: Lupus erythematosus,systemic, Receptors,IgG, Immunoglobulin allotypes