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Evidence from twins for acquired cellular immune hyperactivity in type 1 diabetes
Author(s) -
Petrovsky Nikolai,
Kyvik Kirsten O.,
BonnevieNielsen Vagn,
BeckNielsen Henning,
Green Anders,
Harrison Leonard C.
Publication year - 2002
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2002.01449.x
Subject(s) - immune system , type 2 diabetes , type 1 diabetes , immunology , biology , psychology , diabetes mellitus , developmental psychology , medicine , endocrinology
Summary 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.