Protection against or triggering of Type 1 diabetes? Different roles for viral infections

被引:31
作者
Boettler, Tobias [1 ]
von Herrath, Matthias [1 ]
机构
[1] La Jolla Inst Allergy & Immunol LIAI, La Jolla, CA 92037 USA
关键词
autoimmunity; coxsackievirus; hygiene hypothesis; Type; 1; diabetes; viral infections; BETA-CELL AUTOIMMUNITY; 99TH DAHLEM CONFERENCE; VIRUS-INFECTION; T-CELL; ENTEROVIRUS INFECTION; PANCREATIC-ISLETS; TRANSGENIC MODEL; HEART-DISEASE; RISK-FACTOR; NOD MOUSE;
D O I
10.1586/ECI.10.91
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
The emergence of autoreactivity that ultimately destroys insulin-producing beta-cells and causes Type 1 diabetes (T1D) is a result of genetic susceptibility and environmental factors, such as viral infections. The ability to induce strong cellular immune responses and to cause inflammation in the target organ makes viral infections prime candidates for the initiation of islet autoreactivity. Indeed, certain viruses have been linked to the occurrence of T1D based on epidemiological, serological and histological findings; and several rodent studies clearly demonstrate that viral infections can trigger autoimmunity. However, viruses have also been shown to efficiently prevent autoimmunity, which underlines the beneficial aspects of exposure to microbial agents as suggested by the hygiene hypothesis. Here, we will try to untangle some aspects of the complex interplay between viruses and the immune system and we will recapitulate by what rationale certain viruses have been associated with T1D.
引用
收藏
页码:45 / 53
页数:9
相关论文
共 78 条
[1]
Pathogen recognition and innate immunity [J].
Akira, S ;
Uematsu, S ;
Takeuchi, O .
CELL, 2006, 124 (04) :783-801
[2]
The NOD mouse: A model of immune dysregulation [J].
Anderson, MS ;
Bluestone, JA .
ANNUAL REVIEW OF IMMUNOLOGY, 2005, 23 :447-485
[3]
The NOD mouse model of type 1 diabetes: As good as it gets? [J].
Atkinson, MA ;
Leiter, EH .
NATURE MEDICINE, 1999, 5 (06) :601-604
[4]
CELLULAR-IMMUNITY TO A DETERMINANT COMMON TO GLUTAMATE-DECARBOXYLASE AND COXSACKIE-VIRUS IN INSULIN-DEPENDENT DIABETES [J].
ATKINSON, MA ;
BOWMAN, MA ;
CAMPBELL, L ;
DARROW, BL ;
KAUFMAN, DL ;
MACLAREN, NK .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 94 (05) :2125-2129
[5]
Mechanisms of disease: The effect of infections on susceptibility to autoimmune and allergic diseases [J].
Bach, JF .
NEW ENGLAND JOURNAL OF MEDICINE, 2002, 347 (12) :911-920
[6]
Genetics, pathogenesis and clinical interventions in type 1 diabetes [J].
Bluestone, Jeffrey A. ;
Herold, Kevan ;
Eisenbarth, George .
NATURE, 2010, 464 (7293) :1293-1300
[7]
INSITU CHARACTERIZATION OF AUTOIMMUNE PHENOMENA AND EXPRESSION OF HLA MOLECULES IN THE PANCREAS IN DIABETIC INSULITIS [J].
BOTTAZZO, GF ;
DEAN, BM ;
MCNALLY, JM ;
MACKAY, EH ;
SWIFT, PGF ;
GAMBLE, DR .
NEW ENGLAND JOURNAL OF MEDICINE, 1985, 313 (06) :353-360
[8]
Regulatory T cells selectively express toll-like receptors and are activated by lipopolysaccharide [J].
Caramalho, I ;
Lopes-Carvalho, T ;
Ostler, D ;
Zelenay, S ;
Haury, M ;
Demengeot, J .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (04) :403-411
[9]
A viral epitope that mimics a self antigen can accelerate but nit initiate autoimmune diabetes [J].
Christen, U ;
Edelmann, KH ;
McGavern, DB ;
Wolfe, T ;
Coon, B ;
Teague, MK ;
Miler, SD ;
Oldstone, MBA ;
von Herrath, MG .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (09) :1290-1298
[10]
Immunization in the first month of life may explain decline in incidence of IDDM in the Netherlands [J].
Classen, JB ;
Classen, DC .
AUTOIMMUNITY, 1999, 31 (01) :43-45