Pathogenesis - HLA-DQ7 antigen and resistance to variant CJD

被引：42

作者：

Jackson, GS

Beck, JA

Navarrete, C

Brown, J

Sutton, PM

Contreras, M

Collinge, J

机构：

[1] UCL, Inst Neurol, MRC, Prion Unit, London WC1N 3BG, England

[2] N London Ctr, Natl Blood Serv, London NW9 5BG, England

[3] Royal Free & Univ Coll Med Sch, Dept Immunol, London NW3 2PF, England

[4] Royal Free & Univ Coll Med Sch, Dept Haematol, London NW3 2PF, England

[5] Oxford Radcliffe Hosp, Nuffield Dept Surg, Oxford Transplant Ctr, Oxford OX3 7LJ, England

来源：

NATURE | 2001年 / 414卷 / 6861期

关键词：

D O I：

10.1038/35104694

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Variant Creutzfeldt–Jakob disease (vCJD) in humans is caused by a bovine spongiform encephalopathy (BSE)-like prion strain, and so far about 100 of the many people exposed to BSE prions have developed the condition. Here we show that there is a significantly reduced frequency of the human leukocyte antigen (HLA) class-II type DQ7 in patients with vCJD, but not in those with classical CJD. This apparently protective genetic factor should aid differential diagnosis and may have important implications for understanding host susceptibility to infection by BSE prions, and the distinctive pathogenesis of vCJD, as well as in the identification of targets for prevention and therapy of vCJD.

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页码：269 / 270

页数：2

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