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Int. J. Mol. Sci. 2017, 18(5), 1028; doi:10.3390/ijms18051028

NGF and Its Receptors in the Regulation of Inflammatory Response

1
Division of Rheumatology and Immuno-Rheumatology Research Laboratories, Bambino Gesù Children’s Hospital, 00146 Rome, Italy
2
Institute of Translational Pharmacology, Consiglio Nazionale delle Ricerche (CNR), 00133 Rome, Italy
*
Author to whom correspondence should be addressed.
Academic Editors: Margaret Fahnestock and Keri Martinowich
Received: 17 February 2017 / Revised: 31 March 2017 / Accepted: 3 May 2017 / Published: 11 May 2017
(This article belongs to the Special Issue Neurotrophic Factors—Historical Perspective and New Directions)
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Abstract

There is growing interest in the complex relationship between the nervous and immune systems and how its alteration can affect homeostasis and result in the development of inflammatory diseases. A key mediator in cross-talk between the two systems is nerve growth factor (NGF), which can influence both neuronal cell function and immune cell activity. The up-regulation of NGF described in inflamed tissues of many diseases can regulate innervation and neuronal activity of peripheral neurons, inducing the release of immune-active neuropeptides and neurotransmitters, but can also directly influence innate and adaptive immune responses. Expression of the NGF receptors tropomyosin receptor kinase A (TrkA) and p75 neurotrophin receptor (p75NTR) is dynamically regulated in immune cells, suggesting a varying requirement for NGF depending on their state of differentiation and functional activity. NGF has a variety of effects that can be either pro-inflammatory or anti-inflammatory. This apparent contradiction can be explained by considering NGF as part of an endogenous mechanism that, while activating immune responses, also activates pathways necessary to dampen the inflammatory response and limit tissue damage. Decreases in TrkA expression, such as that recently demonstrated in immune cells of arthritis patients, might prevent the activation by NGF of regulatory feed-back mechanisms, thus contributing to the development and maintenance of chronic inflammation. View Full-Text
Keywords: sensory sympathetic and parasympathetic neurons; neuropeptides; neurotransmitters; innate immunity; inflammatory diseases sensory sympathetic and parasympathetic neurons; neuropeptides; neurotransmitters; innate immunity; inflammatory diseases
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Minnone, G.; De Benedetti, F.; Bracci-Laudiero, L. NGF and Its Receptors in the Regulation of Inflammatory Response. Int. J. Mol. Sci. 2017, 18, 1028.

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