• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

一种乳糜泻激活麦醇溶蛋白肽的无毒类似物:免疫调节的基础?

A non-toxic analogue of a coeliac-activating gliadin peptide: a basis for immunomodulation?

作者信息

Biagi F, Ellis H J, Parnell N D, Shidrawi R G, Thomas P D, O'Reilly N, Corazza G R, Ciclitira P J

机构信息

Gastroenterology Unit, GKT, St. Thomas' Hospital, London, UK.

出版信息

Aliment Pharmacol Ther. 1999 Jul;13(7):945-50. doi: 10.1046/j.1365-2036.1999.00512.x.

DOI:10.1046/j.1365-2036.1999.00512.x
PMID:10383530
Abstract

BACKGROUND

A-gliadin residues 31-49 (peptide A) binds to HLA-DQ2 and is toxic to coeliac small bowel. Analogues of this peptide, which bind to DQ2 molecules but are non-toxic, may be a potential route to inducing tolerance to gliadin in patients with coeliac disease.

METHODS

Toxicity was investigated with small bowel organ culture in six patients with untreated coeliac disease, four with treated coeliac disease and six controls. Analogue peptides comprised alanine substituted variants of peptide A at L31 (peptide D), P36 (E), P38 (F), P39 (G) and P42 (H).

RESULTS

Peptides D and E were toxic in biopsies from some patients. Peptides F, G and H were not toxic.

CONCLUSIONS

Peptide F, which binds to DQ2 more strongly than peptide A, is not toxic in patients with coeliac disease in-vitro; this could be an initial step towards investigation of the induction of tolerance to gliadin in patients affected by coeliac disease.

摘要

背景

α-麦醇溶蛋白残基31 - 49(肽A)与HLA - DQ2结合,对乳糜泻患者的小肠有毒性。该肽的类似物虽能与DQ2分子结合但无毒,可能是诱导乳糜泻患者对麦醇溶蛋白产生耐受性的潜在途径。

方法

在6例未经治疗的乳糜泻患者、4例经治疗的乳糜泻患者和6例对照中,采用小肠器官培养研究毒性。类似物肽包括肽A在L31(肽D)、P36(E)、P38(F)、P39(G)和P42(H)处的丙氨酸取代变体。

结果

肽D和E在一些患者的活检组织中具有毒性。肽F、G和H无毒。

结论

肽F比肽A更强烈地结合DQ2,在体外对乳糜泻患者无毒;这可能是研究诱导乳糜泻患者对麦醇溶蛋白产生耐受性的第一步。

相似文献

1
A non-toxic analogue of a coeliac-activating gliadin peptide: a basis for immunomodulation?一种乳糜泻激活麦醇溶蛋白肽的无毒类似物:免疫调节的基础?
Aliment Pharmacol Ther. 1999 Jul;13(7):945-50. doi: 10.1046/j.1365-2036.1999.00512.x.
2
Characterizing one of the DQ2 candidate epitopes in coeliac disease: A-gliadin 51-70 toxicity assessed using an organ culture system.乳糜泻中DQ2候选表位之一的特征分析:使用器官培养系统评估麦醇溶蛋白A 51 - 70的毒性
Eur J Gastroenterol Hepatol. 2003 Dec;15(12):1293-8. doi: 10.1097/00042737-200312000-00007.
3
An immunodominant DQ8 restricted gliadin peptide activates small intestinal immune response in in vitro cultured mucosa from HLA-DQ8 positive but not HLA-DQ8 negative coeliac patients.一种免疫显性的DQ8限制性麦醇溶蛋白肽可激活来自HLA - DQ8阳性而非HLA - DQ8阴性的乳糜泻患者体外培养黏膜中的小肠免疫反应。
Gut. 2003 Jan;52(1):57-62. doi: 10.1136/gut.52.1.57.
4
In vitro activities of A-gliadin-related synthetic peptides: damaging effect on the atrophic coeliac mucosa and activation of mucosal immune response in the treated coeliac mucosa.麦醇溶蛋白相关合成肽的体外活性:对萎缩性乳糜泻黏膜的损伤作用及对经治疗的乳糜泻黏膜中黏膜免疫反应的激活作用
Scand J Gastroenterol. 1996 Mar;31(3):247-53. doi: 10.3109/00365529609004874.
5
Gliadin specific, HLA DQ2-restricted T cells are commonly found in small intestinal biopsies from coeliac disease patients, but not from controls.麦醇溶蛋白特异性、HLA DQ2限制性T细胞常见于乳糜泻患者的小肠活检组织中,而在对照者中则未发现。
Scand J Immunol. 1997 Sep;46(3):103-9. doi: 10.1046/j.1365-3083.1997.d01-93.x.
6
Gliadin specific, HLA DQ2-restricted T cells are commonly found in small intestinal biopsies from coeliac disease patients, but not from controls.麦醇溶蛋白特异性、HLA DQ2限制性T细胞常见于乳糜泻患者的小肠活检组织中,而在对照者中则未发现。
Scand J Immunol. 1997 Jul;46(1):103-8.
7
Wheat peptide challenge in coeliac disease.乳糜泻中的小麦肽激发试验。
Lancet. 1994 Mar 26;343(8900):758-61. doi: 10.1016/s0140-6736(94)91837-6.
8
Peptide binding characteristics of the coeliac disease-associated DQ(alpha1*0501, beta1*0201) molecule.乳糜泻相关DQ(α1*0501,β1*0201)分子的肽结合特性
Immunogenetics. 1996;44(4):246-53. doi: 10.1007/BF02602553.
9
Refining the rules of gliadin T cell epitope binding to the disease-associated DQ2 molecule in celiac disease: importance of proline spacing and glutamine deamidation.优化乳糜泻中麦醇溶蛋白T细胞表位与疾病相关DQ2分子结合的规则:脯氨酸间距和谷氨酰胺脱酰胺作用的重要性
J Immunol. 2005 Jul 1;175(1):254-61. doi: 10.4049/jimmunol.175.1.254.
10
Structure of celiac disease-associated HLA-DQ8 and non-associated HLA-DQ9 alleles in complex with two disease-specific epitopes.与两种疾病特异性表位复合的乳糜泻相关HLA - DQ8和非相关HLA - DQ9等位基因的结构
Int Immunol. 2000 Aug;12(8):1157-66. doi: 10.1093/intimm/12.8.1157.

引用本文的文献

1
Development of a Sequence Searchable Database of Celiac Disease-Associated Peptides and Proteins for Risk Assessment of Novel Food Proteins.用于新型食品蛋白质风险评估的乳糜泻相关肽和蛋白质序列可搜索数据库的开发
Front Allergy. 2022 May 26;3:900573. doi: 10.3389/falgy.2022.900573. eCollection 2022.
2
Gliadin Peptide Facilitates FITC Dextran Transport across the Non Everted Gut Sac of Rat Small Intestine.麦醇溶蛋白肽促进异硫氰酸荧光素标记的葡聚糖穿过大鼠小肠非外翻肠囊。
Sci Pharm. 2018 Apr 10;86(2):13. doi: 10.3390/scipharm86020013.
3
Diagnostic and Research Aspects of Small Intestinal Disaccharidases in Coeliac Disease.
乳糜泻中小肠双糖酶的诊断和研究方面。
J Immunol Res. 2017;2017:1042606. doi: 10.1155/2017/1042606. Epub 2017 Apr 20.
4
Genome-, Transcriptome- and Proteome-Wide Analyses of the Gliadin Gene Families in Triticum urartu.乌拉尔图小麦醇溶蛋白基因家族的全基因组、转录组和蛋白质组分析
PLoS One. 2015 Jul 1;10(7):e0131559. doi: 10.1371/journal.pone.0131559. eCollection 2015.
5
Parallels between pathogens and gluten peptides in celiac sprue.乳糜泻中病原体与麸质肽之间的相似之处。
PLoS Pathog. 2008 Feb;4(2):e34. doi: 10.1371/journal.ppat.0040034.
6
The immune recognition of gluten in coeliac disease.乳糜泻中麸质的免疫识别
Clin Exp Immunol. 2005 Jun;140(3):408-16. doi: 10.1111/j.1365-2249.2005.02783.x.
7
Coeliac disease: in vivo toxicity of the putative immunodominant epitope.乳糜泻:假定免疫显性表位的体内毒性
Gut. 2003 Dec;52(12):1698-702. doi: 10.1136/gut.52.12.1698.
8
Investigation of the putative immunodominant T cell epitopes in coeliac disease.乳糜泻中假定的免疫显性T细胞表位的研究。
Gut. 2003 Feb;52(2):212-7. doi: 10.1136/gut.52.2.212.