Can infections protect against autoimmunity?

被引:13
作者
Gaisford, Wendy [1 ]
Cooke, Anne [1 ]
机构
[1] Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England
基金
英国惠康基金;
关键词
autoimmunity; helminth; mycobacteria; type; 1; diabetes; REGULATORY T-CELLS; NONOBESE DIABETIC MICE; SALMONELLA-TYPHIMURIUM INFECTION; IMMUNOLOGICAL SELF-TOLERANCE; TRICHURIS-SUIS THERAPY; CENTRAL-NERVOUS-SYSTEM; PRONE NOD MICE; MULTIPLE-SCLEROSIS; ALPHA-GALACTOSYLCERAMIDE; SCHISTOSOMA-MANSONI;
D O I
10.1097/BOR.0b013e32832c2dee
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review It has often been suggested that autoimmune diseases are initiated by certain infectious agents that mimic self-antigens or polyclonally activated autoreactive lymphocytes. An alternative, and not necessarily mutually exclusive, hypothesis that some infections might inhibit the onset of some autoimmune conditions has more recently been explored. In this review, the evidence suggesting that the current rise in the incidence of some autoimmune diseases is attributable to a decrease in the incidence of exposure to certain infections will be discussed. Recent findings Studies using animal models have shown that some infectious agents or products derived from them have the potential to inhibit the onset of autoimmunity. These studies have led to the suggestion that human autoimmune or allergic diseases might be alleviated by the use of microbial products. There are some data that would support such an observation. Summary The incidence of some autoimmune diseases has increased dramatically in recent years in the developed world. Many autoimmune diseases are governed by both genetic and environmental factors. Our immune system has coevolved with infectious agents. There have been marked changes in the exposure to certain infectious agents over the last 70 years. It has been proposed that certain infections of historical importance might inhibit the development of autoimmune disorder. This review highlights studies addressing the ways in which infectious agents might inhibit onset of autoimmunity, and how this might lead to the development of novel therapeutic approaches.
引用
收藏
页码:391 / 396
页数:6
相关论文
共 68 条
[1]   CASE OF HOOKWORM INFESTATION IN A PRECOLUMBIAN AMERICAN [J].
ALLISON, MJ ;
PEZZIA, A ;
HASEGAWA, I ;
GERSZTEN, E .
AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY, 1974, 41 (01) :103-106
[2]  
Alyanakian MA, 2006, DIABETES, V55, P179, DOI 10.2337/diabetes.55.01.06.db05-0189
[3]  
[Anonymous], J LAB CLIN MED
[4]   Trichuris trichiura eggs in the neolithic glacier mummy from the Alps [J].
Aspock, H ;
Auer, H ;
Picher, O .
PARASITOLOGY TODAY, 1996, 12 (07) :255-256
[5]  
BAXTER AG, 1994, IMMUNOLOGY, V83, P227
[6]   Association between alpha beta TCR(+)CD4(-)CD8(-) T-cell deficiency and IDDM in NOD/Lt mice [J].
Baxter, AG ;
Kinder, SJ ;
Hammond, KJL ;
Scollay, R ;
Godfrey, DI .
DIABETES, 1997, 46 (04) :572-582
[7]  
BENNER P, 1985, ADV NURS SCI, V8, P1
[8]   Autoimmunity provoked by infection: how good is the case for T cell epitope mimicry? [J].
Benoist, C ;
Mathis, D .
NATURE IMMUNOLOGY, 2001, 2 (09) :797-801
[9]   Diabetes-prone NOD mice are resistant to Mycobacterium avium and the infection prevents autoimmune disease [J].
Bras, A ;
Aguas, AP .
IMMUNOLOGY, 1996, 89 (01) :20-25
[10]   Functional defects and the influence of age on the frequency of CD4+CD25+ T-Cells in type 1 diabetes [J].
Brusko, TM ;
Wasserfall, CH ;
Clare-Salzler, MJ ;
Schatz, DA ;
Atkinson, MA .
DIABETES, 2005, 54 (05) :1407-1414