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10.1038/s41598-017-11056-9

http://scihub22266oqcxt.onion/10.1038/s41598-017-11056-9
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C5589742!5589742!28883439
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suck abstract from ncbi


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pmid28883439      Sci+Rep 2017 ; 7 (ä): ä
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  • T cells display mitochondria hyperpolarization in human type 1 diabetes #MMPMID28883439
  • Chen J; Chernatynskaya AV; Li JW; Kimbrell MR; Cassidy RJ; Perry DJ; Muir AB; Atkinson MA; Brusko TM; Mathews CE
  • Sci Rep 2017[]; 7 (ä): ä PMID28883439show ga
  • T lymphocytes constitute a major effector cell population in autoimmune type 1 diabetes. Despite essential functions of mitochondria in regulating activation, proliferation, and apoptosis of T cells, little is known regarding T cell metabolism in the progression of human type 1 diabetes. In this study, we report, using two independent cohorts, that T cells from patients with type 1 diabetes exhibited mitochondrial inner-membrane hyperpolarization (MHP). Increased MHP was a general phenotype observed in T cell subsets irrespective of prior antigen exposure, and was not correlated with HbA1C levels, subject age, or duration of diabetes. Elevated T cell MHP was not detected in subjects with type 2 diabetes. T cell MHP was associated with increased activation-induced IFN? production, and activation-induced IFN? was linked to mitochondria-specific ROS production. T cells from subjects with type 1 diabetes also exhibited lower intracellular ATP levels. In conclusion, intrinsic mitochondrial dysfunction observed in type 1 diabetes alters mitochondrial ATP and IFN? production; the latter is correlated with ROS generation. These changes impact T cell bioenergetics and function.
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