β2-adrenergic receptor-mediated negative regulation of group 2 innate lymphoid cell responses Academic Article uri icon

Overview

MeSH Major

  • Cell Transformation, Neoplastic
  • Endothelial Cells
  • Herpesvirus 8, Human
  • Protein Kinases
  • Receptors, Chemokine
  • Tumor Suppressor Proteins
  • Viral Proteins

abstract

  • © 2018 American Association for the Advancement of Science. All rights reserved. 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 β2-adrenergic receptor (β2AR) and colocalize with adrenergic neurons in the intestine. β2AR deficiency resulted in exaggerated ILC2 responses and type 2 inflammation in intestinal and lung tissues. Conversely, β2AR agonist treatment was associated with impaired ILC2 responses and reduced inflammation in vivo. Mechanistically, we demonstrate that the β2AR 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.

publication date

  • March 2, 2018

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1126/science.aan4829

PubMed ID

  • 29496881

Additional Document Info

start page

  • 1056

end page

  • 1061

volume

  • 359

number

  • 6379