Inhibition of diabetes in BB rats by virus infection.

Dyrberg, Thomas; Schwimmbeck, Peter L.; Oldstone, Michael B. A.

doi:10.1172/jci113405

Cited by 60 publications

(24 citation statements)

References 21 publications

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“…Additionally, in this system, increased FasL expression was observed on T cells, and Fas-FasL-mediated T-cell deletion was suggested as a mechanism for the protection from diabetes (31). Virus infection can prevent diabetes in both NOD mice and the BB rat (16,47), and it has been suggested that these infections may alter the trafficking of autoreactive T cells, since infection with lymphocytic choriomeningitis virus enhances the expression of the chemokine IFN-␥-inducible protein 10 in the lymph node draining the pancreas, and it was proposed that this would lead to recruitment of T cells away from the pancreatic islets to the lymph node, where they would undergo apoptosis (10). Th2 cells induced following infection with gastrointestinal helminths result in an upregulation in expression of the integrin ␣4␤7 which binds to the mucosal addressin MAdCAM (32).…”

Section: Discussionmentioning

confidence: 85%

Inhibition of Autoimmune Type 1 Diabetes by Gastrointestinal Helminth Infection

et al. 2007

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Gastrointestinal nematode infections are prevalent worldwide and are potent inducers of T helper 2 responses with the capacity to modulate the immune response to heterologous antigens. Parasitic helminth infection has even been shown to modulate the immune response associated with autoimmune diseases. Nonobese diabetic (NOD) mice provide a model for studying human autoimmune diabetes; as in humans, the development of diabetes in NOD mice has been linked to the loss of self-tolerance to beta cell autoantigens. Previous studies with the NOD mouse have shown that helminth and bacterial infection appears to inhibit type 1 diabetes by disrupting the pathways leading to the Th1-mediated destruction of insulin-producing beta cells. The aim of our study was to examine whether infection with the gastrointestinal helminths Trichinella spiralis or Heligmosomoides polygyrus could inhibit the development of autoimmune diabetes in NOD mice and to analyze the mechanisms involved in protection and the role of Th2 responses. Protection from diabetes was afforded by helminth infection, appeared to inhibit autoimmune diabetes by disrupting pathways leading to the destruction of beta cells, and was mediated by seemingly independent mechanisms depending on the parasite but which may be to be related to the capacity of the host to mount a Th2 response.

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Section: Discussionmentioning

confidence: 85%

Inhibition of Autoimmune Type 1 Diabetes by Gastrointestinal Helminth Infection

et al. 2007

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“…Like the NOD mouse, however, diabetes does occur earlier and with a higher frequency in VAF vivaria than in less clean environments. Deliberate infection with lymphocytic choriomeningitis virus prevents diabetes, perhaps by deleting effector T cells (Dyrberg et al 1988), but infection with Kilham rat virus (KRV 1 ) and other viruses does not affect disease frequency or age at onset ).…”

Section: Translational Modeling Powermentioning

confidence: 99%

Rat Models of Type 1 Diabetes: Genetics, Environment, and Autoimmunity

Mordes

Bortell²,

Blankenhorn³

et al. 2004

ILAR Journal

185

161

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For many years, the vast amount of data gathered from analysis of nonobese diabetic (NOD) and congenic NOD mice has eclipsed interest in the rat for the study of type 1 diabetes. The study of rat models has continued, however, and recently there has been a reanimation of interest for several reasons. First, genetic analysis of the rat has accelerated. Ian4L1, cblb, and Iddm4 are now known to play major roles in rat autoimmunity. Second, rats are amenable to study the interactions of genetics and environment that may be critical for disease expression in humans. Environmental perturbants that predictably enhance the expression of rat autoimmune diabetes include viral infection, toll-like receptor ligation, and depletion of regulatory T cell populations. Finally, data generated in the rat have correctly predicted the outcome of several human diabetes prevention trials, notably the failure of nicotinamide and low dose parenteral and oral insulin therapies.

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“…These include encephalomyocarditis (EMC) virus [41,42], mengo virus [43], reovirus [44] and retrovirus [45][46][47] in mice; Coxsackie B virus, particularly B4, in mice [48,49] and non-human primates [50]; foot-and-mouth virus in pigs and cattle [51]; rubella virus in hamsters and rabbits [52,53]; bovine viral diarrhoea-mucosal disease virus in cattle [54] and Kilham rat virus (KRV) in rats [55]. In addition to inducing diabetes, there is also some evidence that viruses such as lymphocytic choriomeningitis virus (LCMV) [56,57] and mouse hepatitis virus (MHV) [58] can protect against the development of autoimmune T1D in two spontaneously diabetic animals, the BioBreeding (BB) rat and the nonobese diabetic (NOD) mouse.…”

Section: Introductionmentioning

confidence: 99%

A New Look at Viruses in Type 1 Diabetes

Jun¹,

Yoon²

2004

ILAR Journal

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Type 1 diabetes results from the destruction of pancreatic beta cells. Genetic factors are believed to be a major component for the development of type 1diabetes, but the concordance rate for the development of diabetes in identical twins is only about 40%, suggesting that non-genetic factors play an important role in the expression of the disease. Viruses are one environmental factor that is implicated in the pathogenesis of type 1 diabetes. To date, 14 different viruses have been reported to be associated with the development of type 1 diabetes in humans and animal models. Viruses may be involved in the pathogenesis of type 1 diabetes in at least two distinct ways: by inducing beta cellspecific autoimmunity, with or without infection of the beta cells, (e.g. Kilham rat virus) and by cytolytic infection and destruction of the beta cells (e.g. encephalomyocarditis virus in mice). With respect to virus-mediated autoimmunity, retrovirus, reovirus, Kilham rat virus, bovine viral diarrhoea-mucosal disease virus, mumps virus, rubella virus, cytomegalovirus and Epstein-Barr virus are discussed. With respect to the destruction of beta cells by cytolytic infection, encephalomyocarditis virus, mengovirus and Coxsackie B viruses are discussed. In addition, a review of transgenic animal models for virus-induced autoimmune diabetes is included, particularly with regard to lymphocytic choriomeningitis virus, influenza viral proteins and the EpsteinBarr viral receptor. Finally, the prevention of autoimmune diabetes by infection of viruses such as lymphocytic choriomeningitis virus is discussed.

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Inhibition of diabetes in BB rats by virus infection.

Cited by 60 publications

References 21 publications

Inhibition of Autoimmune Type 1 Diabetes by Gastrointestinal Helminth Infection

Inhibition of Autoimmune Type 1 Diabetes by Gastrointestinal Helminth Infection

Rat Models of Type 1 Diabetes: Genetics, Environment, and Autoimmunity

A New Look at Viruses in Type 1 Diabetes

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