Infection is one of the common complications of stroke. It can seriously affect the prognosis of patients. Poststroke infection is closely associated with immune system imbalance, while the excessive activation of sympathetic nerve is an important factor of the occurrence of immunosuppression after stroke. The sympathetic nerve regulates immune cels primarily via β2 adrenergic receptors on the surface of the immune cels. There is evidence to show that β2 adrenergic receptor mediated immune function enhances rather than inhibits under certain conditions, but its specific molecular mechanism is unclear. This article reviews the molecular mechanisms of β2 adrenergic signaling pathway in regulation of inflammation after stroke.