Abstract
Tregs are critical for control of self-reactive T cells that escape thymic selection and end up in the periphery. Treg subsets suppress effector T cell populations through the secretion of immunosuppressive molecules and inhibitory cytokines as well as cell contact-dependent mechanisms. In this issue of the JCI, Wen and colleagues describe another mechanism by which Tregs suppress effector T cell populations. Specifically, the authors reveal that CD8+ T cells in close contact with target T cells release NADPH oxidase 2-containing microvesicles that inhibit TCR activation by elevating ROS and thereby reducing phosphorylation of the TCR-associated kinase ZAP70. Together, the results of this study provide important insight into CD8+ Treg function and into the development of autoimmunity in older individuals.