During chronic inflammation and ageing, the increase in oxidative stress in both intracellular and extracellular compartments is likely to influence local cell functions. Redox changes alter the T-cell proteome in a quantitative and qualitative manner, and post-translational modifications to surface and cytoplasmic proteins by increased reactive species can influence T-cell function. Previously, we have shown that RA (rheumatoid arthritis) T-cells exhibit reduced ROS (reactive oxygen species) production in response to extracellular stimulation compared with age-matched controls, and basal ROS levels [measured as DCF (2′,7′-dichlorofluorescein) fluorescence] are lower in RA T-cells. In contrast, exposing T-cells in vitro to different extracellular redox environments modulates intracellular signalling and enhances cytokine secretion. Together, these data suggest that a complex relationship exists between intra- and extra-cellular redox compartments which contribute to the T-cell phenotype.
Free radicals and redox signalling in T-cells during chronic inflammation and ageing
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Helen R. Griffiths, Christopher R. Dunston, Stuart J. Bennett, Melissa M. Grant, Darren C. Phillips, George D. Kitas; Free radicals and redox signalling in T-cells during chronic inflammation and ageing. Biochem Soc Trans 1 October 2011; 39 (5): 1273–1278. doi: https://doi.org/10.1042/BST0391273
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