Evidence from twins for acquired cellular immune hyperactivity in type 1 diabetes

Nikolai Petrovsky, Kirsten O. Kyvik, Vagn Bonnevie-Nielsen, Henning Beck-Nielsen, Anders Green, Leonard C. Harrison

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)


Type 1 diabetes has been associated with an increased frequency of activated T cells and T-cell hyperactivity to non-specific and disease-specific stimuli including the islet autoantigen glutamic acid decarboxylase 65 (GAD). To address whether T-cell hyperactivity is genetic or acquired we measured whole blood cytokines in vitro in response to GAD or tetanus in 18 identical twin pairs, nine discordant for type 1 diabetes. In addition, the activity of 2′, 5′ oligoadenylate synthetase (OAS) in blood mononuclear cells was measured as a marker of viral infection. Interleukin-2 (IL-2) basally and IL-2 and interferon-γ (IFN-γ) in response to GAD, were detected more frequently and at higher levels in diabetic compared to non-diabetic twins. IL-10 was not different between groups. OAS activity was increased in diabetic compared to non-diabetic twins and showed a correlation with basal IL-2 and GAD-stimulated IFN-γ and IL-10. These findings suggest that T-cell hyperactivity in type 1 diabetes is an acquired trait and could reflect persisting virus expression.

Original languageEnglish
Pages (from-to)584-589
Number of pages6
Issue number4
Publication statusPublished - Aug 2002
Externally publishedYes


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