Tumour Immunology Program, Division of Immunogenetics (D030), German Cancer Research Center (DKFZ), Heidelberg, Germany,
Arch Immunol Ther Exp (Warsz). 2013 Oct;61(5):367-84. doi: 10.1007/s00005-013-0235-0. Epub 2013 Jun 9.
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.
早期的科学报告将活性氧（ROS）的细胞生物学作用仅限于引起病理性损伤。然而，过去十年的广泛研究使得人们广泛认识到细胞内氧化/还原信号是一种重要的稳态调节机制。在已知受氧化还原信号影响的不同细胞过程中，T 细胞激活是最成熟的过程之一。许多研究报告称，ROS 作为 T 细胞受体诱导转录的调节剂是不可或缺的。然而，ROS 触发的信号通路的机制细节还远未阐明。参与生成“氧化信号”的酶源的性质和相互作用也是正在研究的课题。特别是，线粒体呼吸链作为 ROS 产生者的积极参与构成了一个有趣的问题，这对激活的 T 细胞的生物能量学以及 T 细胞介导的病理学都有各种影响。本综述的目的是探讨这些有趣的概念。
