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The Role of Reactive Oxygen Species in Regulating T Cell-mediated Immunity and Disease
Immune Network ; : e14-2018.
Article in English | WPRIM | ID: wpr-740198
Responsible library: WPRO
ABSTRACT
T lymphocytes rely on several metabolic processes to produce the high amounts of energy and metabolites needed to drive clonal expansion and the development of effector functions. However, many of these pathways result in the production of reactive oxygen species (ROS), which have canonically been thought of as cytotoxic agents due to their ability to damage DNA and other subcellular structures. Interestingly, ROS has recently emerged as a critical second messenger for T cell receptor signaling and T cell activation, but the sensitivity of different T cell subsets to ROS varies. Therefore, the tight regulation of ROS production by cellular antioxidant pathways is critical to maintaining proper signal transduction without compromising the integrity of the cell. This review intends to detail the common metabolic sources of intracellular ROS and the mechanisms by which ROS contributes to the development of T cell-mediated immunity. The regulation of ROS levels by the glutathione pathway and the Nrf2-Keap1-Cul3 trimeric complex will be discussed. Finally, T cell-mediated autoimmune diseases exacerbated by defects in ROS regulation will be further examined in order to identify potential therapeutic interventions for these disorders.
Subject(s)

Full text: Available Index: WPRIM (Western Pacific) Main subject: Autoimmune Diseases / DNA / Receptors, Antigen, T-Cell / T-Lymphocytes / Second Messenger Systems / Signal Transduction / Autoimmunity / T-Lymphocyte Subsets / Reactive Oxygen Species / Cytotoxins Language: English Journal: Immune Network Year: 2018 Type: Article
Full text: Available Index: WPRIM (Western Pacific) Main subject: Autoimmune Diseases / DNA / Receptors, Antigen, T-Cell / T-Lymphocytes / Second Messenger Systems / Signal Transduction / Autoimmunity / T-Lymphocyte Subsets / Reactive Oxygen Species / Cytotoxins Language: English Journal: Immune Network Year: 2018 Type: Article