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
- oxidative stress
- reactive oxygen species
- signal transduction
Griffiths, H. R., Dunston, C. R., Bennett, S. J., Grant, M. M., Phillips, D. C., & Kitas, G. D. (2011). Free radicals and redox signalling in T-cells during chronic inflammation and ageing. Biochemical Society Transactions, 39(5), 1273-1278. https://doi.org/10.1042/BST0391273