| First Author | Moriyama S | Year | 2018 |
| Journal | Science | Volume | 359 |
| Issue | 6379 | Pages | 1056-1061 |
| PubMed ID | 29496881 | Mgi Jnum | J:260759 |
| Mgi Id | MGI:6149348 | Doi | 10.1126/science.aan4829 |
| Citation | Moriyama S, et al. (2018) beta2-adrenergic receptor-mediated negative regulation of group 2 innate lymphoid cell responses. Science 359(6379):1056-1061 |
| abstractText | The type 2 inflammatory response is induced by various environmental and infectious stimuli. Although 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 that murine ILC2s express the beta2-adrenergic receptor (beta2AR) and colocalize with adrenergic neurons in the intestine. beta2AR deficiency resulted in exaggerated ILC2 responses and type 2 inflammation in intestinal and lung tissues. Conversely, beta2AR agonist treatment was associated with impaired ILC2 responses and reduced inflammation in vivo. Mechanistically, we demonstrate that the beta2AR pathway is a cell-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 regulatory circuit that limits ILC2-dependent type 2 inflammation. |
