Journal
SCIENCE
Volume 359, Issue 6379, Pages 1056-1061Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aan4829
Keywords
-
Categories
Funding
- Naito Foundation
- Japan Society for the Promotion of Science (JSPS) Overseas Research Fellowships
- Novo Nordic Foundation [14052]
- German Research Foundation [KL 2963/1-1]
- Australian National Health and Medical Research Commission Early Career Fellowship
- Jill Roberts Institute
- Weill Cornell Medicine Pre-Career Award
- NIH [F32-DK109630-01, F32-AI134018-01, AI061570, AI087990, AI074878, AI083480, AI095466, AI095608, AI102942, AI097333]
- European Research Council Advanced Grant [742883]
- Burroughs Wellcome Fund
- Crohn's & Colitis Foundation of America
- European Research Council (ERC) [742883] Funding Source: European Research Council (ERC)
Ask authors/readers for more resources
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 beta(2)-adrenergic receptor (beta(2)AR) and colocalize with adrenergic neurons in the intestine. beta(2)AR deficiency resulted in exaggerated ILC2 responses and type 2 inflammation in intestinal and lung tissues. Conversely, beta(2)AR agonist treatment was associated with impaired ILC2 responses and reduced inflammation in vivo. Mechanistically, we demonstrate that the beta(2)AR 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available