Regulation of T-cell functions by oxidative stress

Abstract

The principal role of adaptive immunity is to distinguish between "self" and "nonself" and thus provide a highly specific line of immunological defence for the efficient removal of foreign material. It comprises of two arms: the effector B-cell arm and effector T-cell arm which act together to remove nonself. The balance between oxidising and reducing agents within these immune cells governs their redox state. This is important as transient controlled changes in the redox state, such as increased production of reactive oxygen species, are vital for signalling and induction of various biological processes, including cell growth and apoptosis. However, in chronic inflammatory diseases, the prolonged and persistent production of ROS, which overwhelms cellular antioxidant systems leading to oxidative stress, may influence T-cell function. This contributes to a T-cell phenotype which is hyporesponsive to growth and death signals and persists at the site of inflammation, perpetuating the immune response. The regulation of T-cell function by oxidative stress therefore has implications for rheumatoid arthritis.