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

Resultado de la investigación: Articlerevisión exhaustiva

178 Citas (Scopus)

Resumen

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.

Idioma originalEnglish (US)
Páginas (desde-hasta)708-711
Número de páginas4
PublicaciónDiabetes
Volumen49
N.º5
DOI
EstadoPublished - may. 2000
Publicado de forma externa

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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