Acceleration of type 1 diabetes by a coxsackievirus infection requires a preexisting critical mass of autoreactive T-cells in pancreatic islets

David V. Serreze, Eric W. Ottendorfer, Tamir M. Elliss, Charles J. Gauntt, Mark A. Atkinson

Research output: Contribution to journalArticlepeer-review

178 Scopus citations

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 β-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 β-cell-autoreactive T-cells has accumulated. Thus, coxsackievirus infections do not appear to initiate β-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.

Original languageEnglish (US)
Pages (from-to)708-711
Number of pages4
JournalDiabetes
Volume49
Issue number5
DOIs
StatePublished - May 2000

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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