Acceleration of type 1 diabetes by a coxsackievirus infection requires a preexisting critical mass of autoreactive T-cells in pancreatic islets [In Process Citation]
Document Type
Article
Publication Date
2000
First Page
708
Last Page
711
JAX Source
Diabetes 2000 May; 49(5):708-11.
Grant
DK46266/DK/NIDDK, DK51090/DK/NIDDK, AI41469/AI/NIAID
Abstract
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. In 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.
Recommended Citation
Serreze DV,
Ottendorfer EW,
Ellis TM,
Gauntt CJ,
Atkinson MA.
Acceleration of type 1 diabetes by a coxsackievirus infection requires a preexisting critical mass of autoreactive T-cells in pancreatic islets [In Process Citation] Diabetes 2000 May; 49(5):708-11.