氧化应激
免疫系统
类风湿性关节炎
免疫学
细胞内
活性氧
细胞生物学
自身免疫性疾病
信号转导
关节炎
生物
医学
抗体
生物化学
出处
期刊:Redox Report
[Informa]
日期:2005-01-01
卷期号:10 (6): 273-280
被引量:94
标识
DOI:10.1179/135100005x83680
摘要
Reactive oxygen species are recognised as important signalling molecules within cells of the immune system. This is, at least in part, due to the reversible activation of kinases, phosphatases and transcription factors by modification of critical thiol residues. However, in the chronic inflammatory disease rheumatoid arthritis, cells of the immune system are exposed to increased levels of oxidative stress and the T cell becomes refractory to growth and death stimuli. This contributes to the perpetuation of the immune response. As many of the effective therapies used in the treatment of rheumatoid arthritis modulate intracellular redox state, this raises the question of whether increased oxidative stress is causative of T-cell hyporesponsiveness. To address this hypothesis, this review considers the putative sources of ROS involved in normal intracellular signalling in T cells and the evidence in support of abnormal ROS fluxes contributing to T-cell hyporesponsiveness.
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