β-Adrenergic signaling blocks murine CD8⁺ T-cell metabolic reprogramming during activation: a mechanism for immunosuppression by adrenergic stress.

ABSTRACT: Primary and secondary lymphoid organs are heavily innervated by the autonomic nervous system. Norepinephrine, the primary neurotransmitter secreted by post-ganglionic sympathetic neurons, binds to and activates β-adrenergic receptors expressed on the surface of immune cells and regulates the functions of these cells. While it is known that both activated and memory CD8⁺ T-cells primarily express the β2-adrenergic receptor (β2-AR) and that signaling through this receptor can inhibit CD8⁺ T-cell effector function, the mechanism(s) underlying this suppression is not understood. Under normal activation conditions, T-cells increase glucose uptake and undergo metabolic reprogramming. In this study, we show that treatment of murine CD8⁺ T-cells with the pan β-AR a

SUBMITTER: Qiao G 

PROVIDER: S-EPMC6326964 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature