Signaling from the nervous system through the β2-adrenergic receptor can help control the type of inflammation that characterizes inflammatory bowel disease (IBD), a new mouse study shows. These findings suggest that new therapies targeting the same pathway as the nervous system may help control inflammation in IBD. The study, “β2-adrenergic receptor–mediated negative regulation of group 2 innate lymphoid cell responses,” was published in the journal Science. Diseases that are characterized by inflammation, such as IBD, tend to exhibit a type of inflammation known as the type 2 inflammatory response, which happens when an individual is exposed to infectious and environmental triggers — helminth infections, allergens, venoms, and other stimuli. One of the main characteristics of the type 2 response is the activation of immune cells called the T helper 2 (TH2) cells, and the release of signaling molecules, called type 2 cytokines, which play major roles in activating the inflammatory response. Recent studies have identified another group of immune cells — called group 2 innate lymphoid cells (ILC2s) — as a potent source of type 2 cytokines and, consequently, contributing to type 2 inflammatory responses. Although considerable advances have been made to define the cytokines and environmental stimuli that trigger ILC2 responses, the regulatory mechanisms that regulate their response and type 2 inflammation are not fully understood. So, researchers conducted a study to determine the regulation of ILC2 responses, looking particularly to the regulation of ILC2 by the central nervous system. ILC2s are activated by a chemical called norepinephrine that is released by nerve cells. Norepinephrine binds to a receptor on the ILC2 surface known