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PLoS One. 2014 Jan 22;9(1):e85086. doi: 10.1371/journal.pone.0085086. eCollection 2014.

Adrenergic β2 receptor activation stimulates anti-inflammatory properties of dendritic cells in vitro.

Author information

1
Tytgat Institute for Gastro-Intestinal and Liver Research, Academic Medical Center, Amsterdam, The Netherlands.
2
Bioceros B.V., Yalelaan 46, Utrecht, The Netherlands.
3
Sanquin Research/Landsteiner Laboratory, Department of Hematopoiesis, Amsterdam, The Netherlands.
4
Laboratory of Pediatric Gastroenterology, Erasmus University Medical Center, Rotterdam, The Netherlands.

Abstract

Vagal nerve efferent activation has been shown to ameliorate the course of many inflammatory disease states. This neuro-modulatory effect has been suggested to rest on acetylcholine receptor (AChR) activation on tissue macrophages or dendritic cells (DCs). In more recent studies, vagal anti-inflammatory activity was shown involve adrenergic, splenic, pathways. Here we provide evidence that the adrenergic, rather than cholinergic, receptor activation on bone marrow derived DCs results in enhanced endocytosis uptake, enhanced IL-10 production but a decreased IL-6, IL-12p70 and IL-23 production. In antigen specific T cell stimulation assays, adrenergic β2 receptor activation on bone marrow DCs led to an enhanced potential to induce Foxp3 positive suppressive Treg cells. These effects were independent of IL10-R activation, TGFβ release, or retinoic acid (RA) secretion. Hence, adrenergic receptor β2 activation modulates DC function resulting in skewing towards anti-inflammatory T cell phenotypes.

PMID:
24465481
PMCID:
PMC3898911
DOI:
10.1371/journal.pone.0085086
[Indexed for MEDLINE]
Free PMC Article

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