Suppr超能文献

乳糜泻中免疫球蛋白增强子HS1,2等位基因2频率增加。

Increased frequency of the immunoglobulin enhancer HS1,2 allele 2 in coeliac disease.

作者信息

Frezza D, Giambra V, Cianci R, Fruscalzo A, Giufrè M, Cammarota G, Martìnez-Labarga C, Rickards O, Scibilia G, Sferlazzas C, Bartolozzi F, Starnino S, Magazzù G, Gasbarrini G B, Pandolfi F

机构信息

Department of Biology, Enrico Calef, Tor Vergata University, IT-00133 Rome, Italy.

出版信息

Scand J Gastroenterol. 2004 Nov;39(11):1083-7. doi: 10.1080/00365520410007999.

Abstract

BACKGROUND

Coeliac disease (CD) is characterized by increased immunological responsiveness to ingested gliadin in genetically predisposed individuals. This genetic predisposition is not completely defined. A dysregulation of immunoglobulins (Ig) is present in CD: since antiendomysium antibodies (anti-EMA) are of the IgA class. One polymorphic enhancer within the locus control region (LCR) of the immunoglobulin heavy chain cluster at the 3' of the C alpha-1 gene was investigated. The correlation of the penetrance of the four different alleles of the HS1,2-A enhancer of the LCR-1 3' to C alpha-1 in CD patients compared to a control population was analysed.

METHODS

A total of 115 consecutive CD outpatients, on a gluten-free diet, and 248 healthy donors, age- and sex-matched, from the same geographical area were enrolled in the study. HS1,2-A allele frequencies were investigated by nested polymerase chain reaction (PCR).

RESULTS

The frequency of allele 2 of the enhancer HS1,2-A gene was increased by 30.8% as compared to the control frequency. The frequency of homozygosity for allele 2 was significantly increased in CD patients. Crude odds ratio (OR) showed that those with 2/2 and 2/4 (OR 2.63, P < 0.001 and OR 2.01, P = 0.03) have a significantly higher risk of developing the disease. In contrast, allele 1/2 may represent a protective genetic factor against CD (OR 0.52, P = 0.01).

CONCLUSIONS

These data provide further evidence of a genetic predisposition in CD. Because of the Ig dysregulation in CD, the enhancer HS1,2-A may be involved in the pathogenesis.

摘要

背景

乳糜泻(CD)的特征是在遗传易感性个体中,对摄入的麦醇溶蛋白的免疫反应性增加。这种遗传易感性尚未完全明确。乳糜泻中存在免疫球蛋白(Ig)失调:因为抗肌内膜抗体(anti-EMA)属于IgA类。研究了位于Cα-1基因3'端的免疫球蛋白重链簇的基因座控制区(LCR)内的一个多态性增强子。分析了LCR-1 3'至Cα-1的HS1,2-A增强子的四种不同等位基因在CD患者中的外显率与对照人群的相关性。

方法

本研究共纳入了115名连续的接受无麸质饮食的CD门诊患者以及248名来自同一地理区域、年龄和性别匹配的健康供体。通过巢式聚合酶链反应(PCR)研究HS1,2-A等位基因频率。

结果

与对照频率相比,增强子HS1,2-A基因的等位基因2的频率增加了30.8%。CD患者中等位基因2的纯合频率显著增加。粗比值比(OR)显示,携带2/2和2/4基因型的个体(OR 2.63,P < 0.001和OR 2.01,P = 0.03)患该病的风险显著更高。相比之下,等位基因1/2可能是针对CD的一种保护性遗传因素(OR 0.52,P = 0.01)。

结论

这些数据为乳糜泻的遗传易感性提供了进一步证据。由于乳糜泻中存在Ig失调,增强子HS1,2-A可能参与了发病机制。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验