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

Titleβ-adrenergic receptor-mediated negative regulation of group 2 innate lymphoid cell responses.
Publication TypeJournal Article
Year of Publication2018
AuthorsMoriyama S, Brestoff JR, Flamar A-L, Moeller JB, Klose CSN, Rankin LC, Yudanin NA, Monticelli LA, Putzel GGarbès, Rodewald H-R, Artis D
JournalScience
Volume359
Issue6379
Pagination1056-1061
Date Published2018 03 02
ISSN1095-9203
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 β-adrenergic receptor (βAR) and colocalize with adrenergic neurons in the intestine. βAR deficiency resulted in exaggerated ILC2 responses and type 2 inflammation in intestinal and lung tissues. Conversely, βAR agonist treatment was associated with impaired ILC2 responses and reduced inflammation in vivo. Mechanistically, we demonstrate that the βAR 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.

DOI10.1126/science.aan4829
Alternate JournalScience
PubMed ID29496881
Grant ListF32 DK109630 / DK / NIDDK NIH HHS / United States
F32 AI134018 / AI / NIAID NIH HHS / United States
R01 AI061570 / AI / NIAID NIH HHS / United States
R21 AI087990 / AI / NIAID NIH HHS / United States
R01 AI074878 / AI / NIAID NIH HHS / United States
R21 AI083480 / AI / NIAID NIH HHS / United States
R01 AI095466 / AI / NIAID NIH HHS / United States
U01 AI095608 / AI / NIAID NIH HHS / United States
R01 AI102942 / AI / NIAID NIH HHS / United States
R01 AI097333 / AI / NIAID NIH HHS / United States