Mouse Models of Virus-Induced Type 1 Diabetes.

@article{Christoffersson2020MouseMO,
  title={Mouse Models of Virus-Induced Type 1 Diabetes.},
  author={Gustaf Christoffersson and Malin Flodstr{\"o}m-Tullberg},
  journal={Methods in molecular biology},
  year={2020},
  volume={2128},
  pages={
          93-105
        }
}
Virus infections have been linked to the induction of autoimmunity and disease development in human type 1 diabetes. Experimental models have been instrumental in deciphering processes leading to break of immunological tolerance and type 1 diabetes development. Animal models have also been useful for proof-of-concept studies and for preclinical testing of new therapeutic interventions. This chapter describes two robust and clinically relevant mouse models for virus-induced type 1 diabetes… 
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References

SHOWING 1-10 OF 34 REFERENCES
Previous maternal infection protects offspring from enterovirus infection and prevents experimental diabetes development in mice
TLDR
Maternally transferred antibodies protect offspring from enterovirus infection and virus-induced diabetes, suggesting that the absence of maternally provided protection increases the risk for severe outcomes after an enterov virus infection in offspring.
Development of the Nonobese Diabetic Mouse and Contribution of Animal Models for Understanding Type 1 Diabetes
TLDR
The history is based on the early literature, mostly written in Japanese, and personal communications especially with Dr Tochino, who was involved in diabetes animal model development and who contributed to the release of NOD mice to the international scientific community.
Acceleration of type 1 diabetes by a coxsackievirus infection requires a preexisting critical mass of autoreactive T-cells in pancreatic islets.
TLDR
It is found that infection with a pancreatrophic coxsackievirus isolate can accelerate type 1 diabetes development through the induction of a bystander activation effect, but only after a critical threshold level of insulitic beta-cell-autoreactive T-cells has accumulated.
Autoimmune Diabetes: An Overview of Experimental Models and Novel Therapeutics.
TLDR
An overview of the experimental models generated and used to gain knowledge on the molecular and cellular mechanisms underlying the breakdown of self-tolerance in T1D and the progression of the autoimmune response is provided.
A Coxsackievirus B vaccine protects against virus-induced diabetes in an experimental mouse model of type 1 diabetes
TLDR
The CVB1 vaccine induced strong neutralising antibody responses and protected against viraemia and the dissemination of virus to the pancreas in both NOD mice and SOCS1-tg mice, indicating that this preclinical proof of concept study provides a base for further studies aimed at developing a vaccine for use in elucidating the role of enteroviruses in human type 1 diabetes.
Target cell defense prevents the development of diabetes after viral infection
TLDR
A fundamental link is established between the responsiveness of target pancreatic β cells to interferons (IFNs) and prevention of coxsackievirus B4 (CVB4)-induced diabetes and alterations in target cell defenses can critically influence susceptibility to disease.
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