Cytokine expression in unstimulated PBMC of children with type 1 diabetes and subjects positive for diabetes‐associated autoantibodies

M Halminen, O Simell, M Knip… - Scandinavian journal of …, 2001 - Wiley Online Library
M Halminen, O Simell, M Knip, J Ilonen
Scandinavian journal of immunology, 2001Wiley Online Library
The aim of this study was to evaluate possible changes in the circulating levels of interferon
(IFN)‐γ, interleukin (IL)‐4 and transforming growth factor (TGF)‐β in association with the
autoimmune process leading to type 1 diabetes. Expression levels of mRNAs specific for
each cytokine were determined in peripheral blood mononuclear cells (PBMC) by a
multiplex reverse transcription–polymerase chain reaction (RT–PCR) followed by
hybridization reactions with lanthanide‐labelled probes and detection by time‐resolved …
The aim of this study was to evaluate possible changes in the circulating levels of interferon (IFN)‐γ, interleukin (IL)‐4 and transforming growth factor (TGF)‐β in association with the autoimmune process leading to type 1 diabetes. Expression levels of mRNAs specific for each cytokine were determined in peripheral blood mononuclear cells (PBMC) by a multiplex reverse transcription–polymerase chain reaction (RT–PCR) followed by hybridization reactions with lanthanide‐labelled probes and detection by time‐resolved fluorometry. Newly diagnosed diabetic children had lower levels of IFN‐γ, IL‐4 and TGF‐β1 signals compared to their age‐ and sex‐matched controls (P < 0.02, P < 0.005 and P < 0.005, respectively) and also the autoantibody‐positive subjects had significantly lower levels of IL‐4 and TGF‐β1 in comparison with their matched controls (P = 0.0013 and P = 0.012). No significant differences were observed when comparing matched pairs of diabetic children and autoantibody‐positive subjects. Our results suggest a systemic bias towards reduced production of T‐helper cell type 2 cytokines (IL‐4 and TGF‐β1) during the autoimmune process, but there was also a reduced level of IFN‐γ expression in the periphery at the onset of clinical diabetes.
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