The type 2 inflammatory response is induced by the exposure to helminth infection, allergens, venoms and other infectious and environmental triggers. The hallmarks of type 2 responses include activation of T helper type 2 cells and release of type 2 cytokines such as interleukin (IL)-4, IL-5, IL-9 and IL-13, production of immunoglobulin E, and the activation and accumulation of multiple immune effector cells such as basophils, mast cells and eosinophils. This cascade of immunologic events is associated with goblet cell hyperplasia, elevated mucus production and induction of smooth muscle contractility. While recent studies identified group 2 innate lymphoid cells (ILC2s) as potent sources of type 2 cytokines, the molecular pathways controlling ILC2 responses are incompletely defined. Here, we demonstrate ILC2s selectively express the β2 adrenergic receptor (β2AR), the receptor for neurotransmitter norepinephrine, and reside in intestinal tissue in close proximity to adrenergic neurons. β2AR-deficiency resulted in exaggerated ILC2 responses and inflammation following helminth infection. Conversely, β2AR agonist-treatment was associated with impaired ILC2 responses and reduced inflammation in vivo. Mechanistically, we demonstrate that the β2AR pathway is an ILC2-intrinsic negative regulator of ILC2 responses through inhibition of cell proliferation and effector function. Collectively, these data provide the first evidence of a neuronal-derived negative regulatory circuit that limits ILC2-dependent type 2 inflammation at mucosal sites.