Yu-Nan Huang1,2, Wei-DE Lin3,4, Pen-Hua Su5,6, DA-Tian Bau7,8, Fuu-Jen Tsai2,3, Chieh-Chen Huang9, Chung-Hsing Wang10,11. 1. Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan, R.O.C. 2. Division of Genetics and Metabolism, Children's Hospital of China Medical University, Taichung, Taiwan, R.O.C. 3. Genetic Center, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan, R.O.C. 4. School of Post Baccalaureate Chinese Medicine, China Medical University, Taichung, Taiwan, R.O.C. 5. Department of Pediatrics, Chung Shan Medical University Hospital, Taichung, Taiwan, R.O.C. 6. School of Medicine, Chung Shan Medical University, Taichung, Taiwan, R.O.C. 7. Terry Fox Cancer Research Laboratory, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan, R.O.C. 8. Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan, R.O.C. 9. Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan, R.O.C.; cchuang@dragon.nchu.edu.tw Chwang5894@gmail.com. 10. Division of Genetics and Metabolism, Children's Hospital of China Medical University, Taichung, Taiwan, R.O.C.; cchuang@dragon.nchu.edu.tw Chwang5894@gmail.com. 11. School of Medicine, China Medical University, Taichung, Taiwan, R.O.C.
Abstract
BACKGROUND/AIM: The T cell's flexibility of the immune system to be regulated affects the onset of type 1 diabetes (T1D). However, the mechanisms of endoplasmic reticulum (ER) stress and inflammasome activation in the circulating CD3+CD56+ T cells of patients with T1D remain unclear. This study evaluated the role of CD3+CD56+ T cells in T1D and their correlations with ER stress, inflammasome activation and disease characteristics. MATERIALS AND METHODS: The frequency of circulating CD3+CD56+ T cells was determined using flow cytometry in healthy individuals and patients with T1D. Calnexin, NLR family pyrin domain containing 3 (NLRP3), ASC, caspase-1 (Casp1), cleaved caspase-3 (C-Casp3), and annexin V (AnnV) expression and propidium iodide staining in CD3+/CD56+ T cells were analyzed using flow cytometry. RESULTS: The frequency of CD3+CD56+ T cells was reduced in patients with T1D relative to that in healthy individuals. In addition, high calnexin, NLRP3, ASC and Casp1 expression in CD3+CD56+ T cells was negatively correlated with the percentage of CD3+CD56+ T cells in patients with T1D. CONCLUSION: ER stress, inflammasome activation, and a lower peripheral frequency of circulating CD3+CD56+ T cells might indicate disease progression and necessitate clinical T1D immunological self-tolerance monitoring.
BACKGROUND/AIM: The T cell's flexibility of the immune system to be regulated affects the onset of type 1 diabetes (T1D). However, the mechanisms of endoplasmic reticulum (ER) stress and inflammasome activation in the circulating CD3+CD56+ T cells of patients with T1D remain unclear. This study evaluated the role of CD3+CD56+ T cells in T1D and their correlations with ER stress, inflammasome activation and disease characteristics. MATERIALS AND METHODS: The frequency of circulating CD3+CD56+ T cells was determined using flow cytometry in healthy individuals and patients with T1D. Calnexin, NLR family pyrin domain containing 3 (NLRP3), ASC, caspase-1 (Casp1), cleaved caspase-3 (C-Casp3), and annexin V (AnnV) expression and propidium iodide staining in CD3+/CD56+ T cells were analyzed using flow cytometry. RESULTS: The frequency of CD3+CD56+ T cells was reduced in patients with T1D relative to that in healthy individuals. In addition, high calnexin, NLRP3, ASC and Casp1 expression in CD3+CD56+ T cells was negatively correlated with the percentage of CD3+CD56+ T cells in patients with T1D. CONCLUSION: ER stress, inflammasome activation, and a lower peripheral frequency of circulating CD3+CD56+ T cells might indicate disease progression and necessitate clinical T1D immunological self-tolerance monitoring.
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