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.