共 124 条
Coxsackievirus B4 and type 1 diabetes pathogenesis: contribution of animal models
被引:45
作者:
Jaidane, H.
[1
,2
]
Sane, F.
[1
]
Gharbi, J.
[2
]
Aouni, M.
[2
]
Romond, M. B.
[1
]
Hober, D.
[1
]
机构:
[1] Univ Lille 2, Ctr Biol Pathol & Eurasante, CHRU Lille,Lab Virol UPRES,Fac Med, Pathogenese & Virale Diabet Type 1 EA3610, F-59037 Lille, France
[2] Fac Pharm Monastir, Unite Pathogenese & Virulence Virales, Lab Virol LR99ES27, Monastir 5000, Tunisia
关键词:
type 1 diabetes (T1D);
pathogenesis;
coxsackievirus B (CV-B);
animal models;
64,000-MR ISLET AUTOANTIGEN;
BETA-CELL AUTOIMMUNITY;
AUTOREACTIVE T-CELLS;
ENTEROVIRUS RNA;
PANCREATIC-ISLETS;
VIRAL-INFECTIONS;
RISK-FACTOR;
GLUTAMATE-DECARBOXYLASE;
LEW.1AR1/ZTM-IDDM RAT;
VIRUS-INFECTIONS;
D O I:
10.1002/dmrr.995
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
The role of enteroviruses, in particular type B coxsackieviruses (CV-B), in type 1 diabetes (T1D) pathogenesis is supported by epidemiological, clinical and experimental observations. The investigation of T1D pathogenesis benefits from the contribution of animal models called spontaneously diabetic. Among these animals the non-obese diabetic (NOD) mouse and the bio-breeding diabetes-prone (BBDP) rat present a genetic susceptibility manifested by the expression of an autoimmune diabetes similar to the pathology observed in human beings. Other models whose genetic predisposition is less known are of considerable contribution as well. Numerous major observations relative to several aspects of T1D pathogenesis in the context of CV-B infections, such as susceptibility, diabetogenicity, pancreatotropism, mechanisms of p cells destruction and others, have been deduced thanks to investigations with animal models. Despite their limits, these models are necessary in improving our knowledge of the role of enteroviruses, like CV-B4, in the pathogenesis of T1D, and the recent advances ensuing from their contribution may have important therapeutic and preventive spin-offs. Copyright (C) 2009 John Wiley & Sons, Ltd.
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页码:591 / 603
页数:13
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