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. 2002 Aug;106(4):584-9.
doi: 10.1046/j.1365-2567.2002.01449.x.

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

Nikolai Petrovsky  1 , Kirsten O Kyvik, Vagn Bonnevie-Nielsen, Henning Beck-Nielsen, Anders Green, Leonard C Harrison
Affiliations

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

Nikolai Petrovsky et al. Immunology. 2002 Aug.

Abstract

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-gamma (IFN-gamma) 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-gamma and IL-10. These findings suggest that T-cell hyperactivity in type 1 diabetes is an acquired trait and could reflect persisting virus expression.

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Figures

Figure 1
Figure 1
IL-2 production during 48 hr in whole blood from non-diabetic (ND) and diabetic (D) twins.
Figure 2
Figure 2
Cytokine production during 48 hr in whole blood from non-diabetic (ND) and diabetic (D) twins, in the presence of glutamic acid decarboxylase 65 (GAD 65) at 10 µg/ml.
Figure 3
Figure 3
Cytokine production during 48 hr in whole blood from non-diabetic (ND) and diabetic (D) twins, in the presence of tetanus toxoid at 10 L.f.u./ml.
See this image and copyright information in PMC

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