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乳糜泻:假定免疫显性表位的体内毒性

Coeliac disease: in vivo toxicity of the putative immunodominant epitope.

作者信息

Fraser J S, Engel W, Ellis H J, Moodie S J, Pollock E L, Wieser H, Ciclitira P J

机构信息

Gastroenterology Department, Rayne Institute (KCL), St Thomas' Hospital, London SE1 7EH, UK.

出版信息

Gut. 2003 Dec;52(12):1698-702. doi: 10.1136/gut.52.12.1698.

Abstract

BACKGROUND

Peptides from alpha-gliadins have been used to characterise the immunodominant coeliac toxic epitope. A peptide corresponding to amino acid residues 57-73 of A-gliadin causes peripheral blood mononuclear cells from coeliac patients to secrete interferon gamma (IFN-gamma); gluten specific small intestinal T cell clones proliferate in response to peptides corresponding to residues 57-68 and 62-75 of alpha-gliadins. We wished to investigate whether a peptide corresponding to residues 56-75 of alpha-gliadins exacerbates coeliac disease in vivo.

METHODS

Four adults with coeliac disease, all of whom were on a gluten free diet, underwent three challenges. Peptic-tryptic gliadin (PTG 1 g) served as a positive control. The test peptide and a negative control peptide were studied on separate occasions. The peptides were instilled into the duodenum and biopsies were taken before the infusion, and two, four, and six hours after commencing the infusions, using a Quinton hydraulic multiple biopsy capsule. Biopsy specimens were assessed blindly for villus height to crypt depth ratio (VH:CD), enterocyte cell height (ECH), and intraepithelial lymphocyte (IEL) count. We used the Mann-Whitney U test, with 95% confidence intervals, for statistical analysis.

RESULTS

VH:CD and ECH fell, and IEL increased significantly 4-6 hours after commencing infusions with both PTG and the test peptide in all subjects. The negative control peptide caused no significant changes to villus morphology, enterocyte height, or IEL count in any patient.

CONCLUSION

We have confirmed that the putative immunodominant epitope, a peptide corresponding to residues 56-75 of alpha-gliadins, exacerbates coeliac disease in vivo.

摘要

背景

来自α-麦醇溶蛋白的肽已被用于鉴定免疫显性的乳糜泻毒性表位。一种对应于A-麦醇溶蛋白氨基酸残基57 - 73的肽可使乳糜泻患者的外周血单核细胞分泌γ-干扰素(IFN-γ);麸质特异性小肠T细胞克隆可对对应于α-麦醇溶蛋白残基57 - 68和62 - 75的肽产生增殖反应。我们希望研究一种对应于α-麦醇溶蛋白残基56 - 75的肽在体内是否会加重乳糜泻。

方法

4名患有乳糜泻的成年人,均采用无麸质饮食,接受了三次激发试验。胃蛋白酶-胰蛋白酶处理的麦醇溶蛋白(PTG 1 g)作为阳性对照。在不同时间分别研究测试肽和阴性对照肽。将肽注入十二指肠,并在注入前以及注入开始后2小时、4小时和6小时,使用昆顿液压多活检胶囊进行活检。对活检标本进行盲法评估,以确定绒毛高度与隐窝深度之比(VH:CD)、肠上皮细胞高度(ECH)和上皮内淋巴细胞(IEL)计数。我们使用曼-惠特尼U检验及95%置信区间进行统计分析。

结果

在所有受试者中,开始注入PTG和测试肽后4 - 6小时,VH:CD和ECH下降,IEL显著增加。阴性对照肽在任何患者中均未引起绒毛形态、肠上皮细胞高度或IEL计数的显著变化。

结论

我们已证实,假定的免疫显性表位,即一种对应于α-麦醇溶蛋白残基56 - 75的肽,在体内会加重乳糜泻。

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Molecular basis of celiac disease.乳糜泻的分子基础。
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