Mitochondria as Oxidative Signaling Organelles in T-cell Activation: Physiological Role and Pathological Implications

作者：Kaminski Marcin M^*; Roeth Daniel; Krammer Peter H; Guelow Karsten

来源：Archivum Immunologiae et Therapiae Experimentalis, 2013, 61(5): 367-384.

DOI：10.1007/s00005-013-0235-0

• Reactive oxygen species (ROS)
• Complex I (NADH:ubiquinone oxidoreductase)
• T-cell receptor (TCR)
• NF-kappaB (NF-kappa B)
• Glycerol-3-phosphate dehydrogenase (GPD2)
• ADP-dependent glucokinase (ADPGK)

Early scientific reports limited the cell biological role of reactive oxygen species (ROS) to the cause of pathological damage. However, extensive research performed over the last decade led to a wide recognition of intracellular oxidative/redox signaling as a crucial mechanism of homeostatic regulation. Amongst different cellular processes known to be influenced by redox signaling, T-cell activation is one of the most established. Numerous studies reported an indispensible role for ROS as modulators of T-cell receptor-induced transcription. Nevertheless, mechanistic details regarding signaling pathways triggered by ROS are far from being delineated. The nature and interplay between enzymatic sources involved in the generation of "oxidative signals" are also a matter of ongoing research. In particular, active participation of the mitochondrial respiratory chain as ROS producer constitutes an intriguing issue with various implications for bioenergetics of activated T cells as well as for T-cell-mediated pathologies. The aim of the current review is to address these interesting concepts.

• 出版日期2013-10