Acceleration of type 1 diabetes by a coxsackievirus infection requires a preexisting critical mass of autoreactive T-cells in pancreatic islets
| Autor: | Mark A. Atkinson, David V. Serreze, Charles J. Gauntt, Eric W. Ottendorfer, Tamir M. Ellis |
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| Rok vydání: | 2000 |
| Předmět: |
Time Factors
Endocrinology Diabetes and Metabolism T-Lymphocytes Coxsackievirus Infections Inflammation Autoimmunity Mice SCID Biology Coxsackievirus Islets of Langerhans Mice Immunity Mice Inbred NOD Internal Medicine medicine Bystander effect Animals Pancreas Autoimmune disease Type 1 diabetes Pancreatic islets medicine.disease biology.organism_classification medicine.anatomical_structure Diabetes Mellitus Type 1 Immunology Disease Progression medicine.symptom |
| Zdroj: | Diabetes. 49(5) |
| ISSN: | 0012-1797 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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