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将爱泼斯坦-巴尔病毒BOLF1分子与HLA-DQw8β链之间的同源性与近期起病的1型(胰岛素依赖型)糖尿病联系起来。

Relating homology between the Epstein-Barr virus BOLF1 molecule and HLA-DQw8 beta chain to recent onset type 1 (insulin-dependent) diabetes mellitus.

作者信息

Sairenji T, Daibata M, Sorli C H, Qvistbäck H, Humphreys R E, Ludvigsson J, Palmer J, Landin-Olsson M, Sundkvist G, Michelsen B

机构信息

Department of Pharmacology and Medicine, University of Massachusetts Medical School, Worcester.

出版信息

Diabetologia. 1991 Jan;34(1):33-9. doi: 10.1007/BF00404022.

Abstract

A role for the Epstein-Barr virus in initiating Type 1 (insulin-dependent) diabetes mellitus has been proposed since Epstein-Barr virus BOLF1 (497-513) AVTPL RIFIVPPAAEY has an 11 amino acid identity with HLA-DQw8 beta (49-60) AVTPL GPPAAEY. Rabbit antisera to the BOLF1 (496-515) peptide crossreacted with the homologous DQw8 beta (44-63) peptide but not with the related DQw7 beta (44-63) peptide, which differed from the DQw8 peptide only in an ALA to ASP substitution in position 57. Antisera to DQw8 beta (49-60) reacted with the DQw8 beta (44-63) peptide and BOLF1 (496-515), but not with DQw7 beta (44-63). The antiserum to the BOLF1 peptide bound to denatured class II major histocompatibility complex beta chains from Epstein-Barr virus-transformed DQw8-positive lymphocytes in an immunoblotting analysis. Epstein-Barr virus antibodies were detected at equal frequencies and similar titres in sera of 30 patients with Type 1 diabetes (16 of 30; 63%) and in sera of 20 non-diabetic control subjects (13 of 20; 65%). Sera from diabetic patients did not bind to DQw8 beta (44-63) or BOLF1 (496-515) peptides. From these data we conclude that there is no simple relationship between serological evidence of Epstein-Barr virus infection and crossreactions between homologous Epstein-Barr virus and class II major histocompatibility complex peptides.

摘要

自发现爱泼斯坦-巴尔病毒BOLF1 (497 - 513) AVTPL RIFIVPPAAEY与HLA - DQw8β (49 - 60) AVTPL GPPAAEY有11个氨基酸相同以来,有人提出爱泼斯坦-巴尔病毒在引发1型(胰岛素依赖型)糖尿病中起作用。针对BOLF1 (496 - 515)肽段的兔抗血清与同源的DQw8β (44 - 63)肽段发生交叉反应,但与相关的DQw7β (44 - 63)肽段不发生交叉反应,后者与DQw8肽段仅在第57位的丙氨酸被天冬氨酸取代。针对DQw8β (49 - 60)的抗血清与DQw8β (44 - 63)肽段和BOLF1 (496 - 515)发生反应,但与DQw7β (44 - 63)不发生反应。在免疫印迹分析中,针对BOLF1肽段的抗血清与来自爱泼斯坦-巴尔病毒转化的DQw8阳性淋巴细胞的变性II类主要组织相容性复合体β链结合。在30例1型糖尿病患者的血清(30例中的16例;63%)和20例非糖尿病对照受试者的血清(20例中的13例;65%)中,检测到爱泼斯坦-巴尔病毒抗体的频率和滴度相同。糖尿病患者的血清不与DQw8β (44 - 63)或BOLF1 (496 - 515)肽段结合。从这些数据我们得出结论,爱泼斯坦-巴尔病毒感染的血清学证据与同源的爱泼斯坦-巴尔病毒和II类主要组织相容性复合体肽段之间的交叉反应之间没有简单的关系。

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