β 2 -adrenergic receptor–mediated negative regulation of group 2 innate lymphoid cell responses

• DOI: 10.1126/science.aan4829
• Publication Date: 2018-03-01T19:05:42Z
• Authors: Saya Moriyama; Jonathan R. Brestoff; Anne-Laure Flamar; Jesper B. Moeller; Christoph S. N. K...; Lucille C. Rankin; Naomi A. Yudanin; Laurel A. Monticelli; Gregory Garbès Pu...; Hans-Reimer Rodewald; David Artis
• Keywords: Innate lymphoid cell

The type 2 inflammatory response is induced by various environmental and infectious stimuli. Although recent studies identified group innate lymphoid cells (ILC2s) as potent sources of cytokines, the molecular pathways controlling ILC2 responses are incompletely defined. Here we demonstrate that murine ILC2s express β2-adrenergic receptor (β2AR) colocalize with adrenergic neurons in intestine. β2AR deficiency resulted exaggerated inflammation intestinal lung tissues. Conversely, agonist treatment was associated impaired reduced vivo. Mechanistically, pathway a cell-intrinsic negative regulator through inhibition cell proliferation effector function. Collectively, these data provide first evidence neuronal-derived regulatory circuit limits ILC2-dependent inflammation.