ß2-adrenergic receptor-mediated negative regulation of group 2 innate lymphoid cell responses.
Science
; 359(6379): 1056-1061, 2018 03 02.
Article
in En
| MEDLINE
| ID: mdl-29496881
ABSTRACT
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 ß2-adrenergic receptor (ß2AR) and colocalize with adrenergic neurons in the intestine. ß2AR deficiency resulted in exaggerated ILC2 responses and type 2 inflammation in intestinal and lung tissues. Conversely, ß2AR agonist treatment was associated with impaired ILC2 responses and reduced inflammation in vivo. Mechanistically, we demonstrate that the ß2AR 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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Lymphocytes
/
Receptors, Adrenergic, beta-2
/
Adaptive Immunity
/
Adrenergic Neurons
/
Immunity, Innate
Limits:
Animals
/
Humans
Language:
En
Journal:
Science
Year:
2018
Document type:
Article
Affiliation country:
Estados Unidos