Journal
DIABETES
Volume 49, Issue 5, Pages 708-711Publisher
AMER DIABETES ASSOC
DOI: 10.2337/diabetes.49.5.708
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- NIAID NIH HHS [AI41469] Funding Source: Medline
- NIDDK NIH HHS [DK51090, DK46266] Funding Source: Medline
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Coxsackievirus infections have been proposed as an environmental trigger for the development of T-cell-mediated autoimmune (type 1) diabetes by either providing a molecular mimic of the candidate pancreatic beta-cell autoantigen GAD or inducing bystander inflammation in the pancreas, Tn this study in the NOD mouse model, we 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, Thus, coxsackievirus infections do not: appear to initiate beta-cell autoreactive immunity but can accelerate the process once it is underway. These findings indicate that the timing of a coxsackievirus infection, rather than its simple presence or absence, may have important etiological implications for the development of T-cell-mediated autoimmune type 1 diabetes in humans.
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