LAUSR

Cellular redox homeostasis plays a pivotal role in generation and maintenance of physiological responses. Perturbation in cellular redox status causes modulation in redox sensitive signaling pathways determining the cell fate. Depending on the extent of generation and spatio-temporal regulation of reactive oxygen species (ROS) generating oxidative stress, it can act as death stimulus or as secondary messenger. Multiple exogenous oxidants or thiol reactive compounds, endogenous oxidants such as NADPH oxidase, superoxide dismutase regulate T cell mediated immune responses. Thus, a meticulous understanding of the coordinated functioning of T cell mediated immune responses in oxidative niche is essential. The present review aims to delineate the effect of cellular redox status on T cell activation and subsequent regulation of redox sensitive immunoregulatory transcription factors such as NF-κB, NFAT and AP-1, which manifests the onset of inflammation associated disorders.