Antiviral immune responses: triggers of or triggered by autoimmunity?

被引：359

作者：

Muenz, Christian ^{[1
,2
]}

Luenemann, Jan D. ^{[2
]}

Getts, Meghann Teague ^{[3
,4
]}

Miller, Stephen D. ^{[3
,4
]}

机构：

[1] Univ Zurich Hosp, Inst Expt Immunol, CH-8057 Zurich, Switzerland

[2] Rockefeller Univ, Lab Viral Immunobiol, New York, NY 10065 USA

[3] Northwestern Univ, Dept Microbiol Immunol, Feinberg Sch Med, Chicago, IL 60611 USA

[4] Northwestern Univ, Interdept Immunobiol Ctr, Feinberg Sch Med, Chicago, IL 60611 USA

来源：

NATURE REVIEWS IMMUNOLOGY | 2009年 / 9卷 / 04期

基金：

美国国家卫生研究院;

关键词：

EPSTEIN-BARR-VIRUS; CENTRAL-NERVOUS-SYSTEM; MYELIN BASIC-PROTEIN; AUTOREACTIVE T-CELLS; GLUTAMIC-ACID DECARBOXYLASE; DEPENDENT DIABETES-MELLITUS; MULTIPLE-SCLEROSIS PATIENTS; ACTIVATE B-CELLS; MOLECULAR MIMICRY; LUPUS-ERYTHEMATOSUS;

D O I：

10.1038/nri2527

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The predisposition of individuals to several common autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis, is genetically linked to certain human MHC class II molecules and other immune modulators. However, genetic predisposition is only one risk factor for the development of these diseases, and low concordance rates in monozygotic twins, as well as the geographical distribution of disease risk, suggest the involvement of environmental factors in the development of these diseases. Among these environmental factors, infections have been implicated in the onset and/or promotion of autoimmunity. In this Review, we outline the mechanisms by which viral infection can trigger autoimmune disease and describe the pathways by which infection and immune control of infectious disease might be dysregulated during autoimmunity.

引用

页码：246 / 258

页数：13

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