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Int. J. Mol. Sci. 2015, 16(3), 5635-5665; doi:10.3390/ijms16035635

Molecular Mechanisms Underlying β-Adrenergic Receptor-Mediated Cross-Talk between Sympathetic Neurons and Immune Cells

1
College of Arts and Sciences, Kent State University, Kent, OH 44304, USA
2
Department of Human Anatomy and Pathology, Loma Linda University, School of Medicine, Loma Linda, CA 92350, USA
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: Jens Schlossmann
Received: 4 December 2014 / Revised: 13 February 2015 / Accepted: 4 March 2015 / Published: 11 March 2015
(This article belongs to the Special Issue Signalling Molecules and Signal Transduction in Cells 2014)
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Abstract

Cross-talk between the sympathetic nervous system (SNS) and immune system is vital for health and well-being. Infection, tissue injury and inflammation raise firing rates of sympathetic nerves, increasing their release of norepinephrine (NE) in lymphoid organs and tissues. NE stimulation of β2-adrenergic receptors (ARs) in immune cells activates the cAMP-protein kinase A (PKA) intracellular signaling pathway, a pathway that interfaces with other signaling pathways that regulate proliferation, differentiation, maturation and effector functions in immune cells. Immune–SNS cross-talk is required to maintain homeostasis under normal conditions, to develop an immune response of appropriate magnitude after injury or immune challenge, and subsequently restore homeostasis. Typically, β2-AR-induced cAMP is immunosuppressive. However, many studies report actions of β2-AR stimulation in immune cells that are inconsistent with typical cAMP–PKA signal transduction. Research during the last decade in non-immune organs, has unveiled novel alternative signaling mechanisms induced by β2-AR activation, such as a signaling switch from cAMP–PKA to mitogen-activated protein kinase (MAPK) pathways. If alternative signaling occurs in immune cells, it may explain inconsistent findings of sympathetic regulation of immune function. Here, we review β2-AR signaling, assess the available evidence for alternative signaling in immune cells, and provide insight into the circumstances necessary for “signal switching” in immune cells. View Full-Text
Keywords: Neural–immune interactions; stress; β2-adrenergic receptor signaling; GRK; β-arrestin; PKA; ERK1/2; receptor regulation; innate and adaptive immunity Neural–immune interactions; stress; β2-adrenergic receptor signaling; GRK; β-arrestin; PKA; ERK1/2; receptor regulation; innate and adaptive immunity
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Lorton, D.; Bellinger, D.L. Molecular Mechanisms Underlying β-Adrenergic Receptor-Mediated Cross-Talk between Sympathetic Neurons and Immune Cells. Int. J. Mol. Sci. 2015, 16, 5635-5665.

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