Mechanisms and Therapeutic Relevance of Neuro-immune Communication

Chavan, Sangeeta S.; Pavlov, Valentin A.; Tracey, Kevin J.

doi:10.1016/j.immuni.2017.06.008

Cited by 480 publications

(398 citation statements)

References 162 publications

Supporting

Mentioning

359

Contrasting

Unclassified

Order By: Relevance

“…Somatosensory neurons have their peripheral axons in the skin, joints, and muscles, whereas visceral neurons innervate the gastrointestinal tract, liver, pancreas, lungs, heart, and other organs. Both types of neurons project to the spinal cord via the dorsal horn and synapse with interneurons and relay neurons transmitting the signals to the brain (17, 18). Vagus nerve sensory (visceral) neurons are localized in the nodose and jugular ganglia.…”

Section: Neurocentric Perspectivesmentioning

confidence: 99%

“…Ongoing research provides important insight into neuro-immune communication with translational relevance (18, 113). In this section we briefly outline current clinical studies stemming from this research and exploring relevant pharmacological modalities and bioelectronic neuromodulation as novel therapeutics for inflammatory and autoimmune conditions.…”

Section: Clinical Translation Of Neuroscience In Inflammatory Diseasementioning

confidence: 99%

“…The release of neuropeptides, including calcitonin gene-related peptide (CGRP), galanin, somatostatin, substance P, and vasoactive intestinal peptide (VIP) in an axon-reflex fashion regulates immune responses. Some components of this figure are adapted from Reference 18.…”

Section: Figurementioning

confidence: 99%

“…Norepinephrine and epinephrine bind to the β 2 -adrenergic receptors on macrophages and other immune cells and induce intracellular signaling, involving cyclic AMP and protein kinase A (PKA), which results in suppression of NF-κB activity and proinflammatory cytokine release. Some components of this figure are adapted from Reference 18. Other abbreviations: cAMP, cyclic adenosine monophosphate; DMN, dorsal motor nucleus of the vagus; mt, mitochondrial; PRR, pattern recognition receptor.…”

Section: Figurementioning

confidence: 99%

See 3 more Smart Citations

Molecular and Functional Neuroscience in Immunity

Pavlov

Chavan

Tracey

2018

Annu. Rev. Immunol.

Self Cite

333

320

View full text Add to dashboard Cite

The nervous system regulates immunity and inflammation. The molecular detection of pathogen fragments, cytokines, and other immune molecules by sensory neurons generates immunoregulatory responses through efferent autonomic neuron signaling. The functional organization of this neural control is based on principles of reflex regulation. Reflexes involving the vagus nerve and other nerves have been therapeutically explored in models of inflammatory and autoimmune conditions, and recently in clinical settings. The brain integrates neuro-immune communication, and brain function is altered in diseases characterized by peripheral immune dysregulation and inflammation. Here we review the anatomical and molecular basis of the neural interface with immunity, focusing on peripheral neural control of immune functions and the role of the brain in the model of the immunological homunculus. Clinical advances stemming from this knowledge within the framework of bioelectronic medicine are also briefly outlined.

show abstract

Section: Neurocentric Perspectivesmentioning

confidence: 99%

Section: Clinical Translation Of Neuroscience In Inflammatory Diseasementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

See 2 more Smart Citations

Molecular and Functional Neuroscience in Immunity

Pavlov

Chavan

Tracey

2018

Annu. Rev. Immunol.

Self Cite

333

320

View full text Add to dashboard Cite

show abstract

“…Latest advances have shown that the nervous system has a close relationship with the immune system, and neuroimmune communications are essential to regulate immune function in response to pathological conditions [12, 13]. The sympathetic nervous system (SNS) communicates with all cells of the immune system, regulating their function through the release of norepinephrine (NE), and activating intercellular signaling pathway via the adrenergic receptors (ARs) expressed on immunocytes [13, 14].…”

Section: Introductionmentioning

confidence: 99%

Acute Traumatic Brain Injury Induces CD4<sup>+</sup> and CD8<sup>+</sup> T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

Yang

Chen

et al. 2019

Neuroimmunomodulation

View full text Add to dashboard Cite

Objective: Traumatic brain injury (TBI) induces immunosuppression in the acute phase, and the activation of the sympathetic nervous system (SNS) might play a role in this process, but the mechanism involved is unknown. Herein, we explored the impact of acute (a)TBI on the peripheral immune system and its correlation with the SNS and the T cell exhaustion marker, PD-1 (programmed cell death-1). Methods: Flow cytometry (FCM) was performed to analyze the expression of T cell markers and intracellular cytokines, interferon-γ and tumor necrosis factor-α, and the T cell exhaustion marker, PD-1, in the peripheral blood mononuclear cells (PBMCs) of TBI rats. Enzyme-linked immunosorbent assay (ELISA) was performed to analyze the concentration of norepinephrine (NE) in the serum. Propranolol was administrated to block the SNS in vivo and NE stimulation was used to imitate the activation of the SNS in vitro. Results: We found that the concentration of NE was significantly elevated after TBI, and the dysfunction of CD4⁺ and CD8⁺ T cells was reversed by the SNS blocker propranolol in vivo and imitated by the SNS neurotransmitter NE in vitro. The expression of PD-1 on CD4⁺ and CD8⁺ T cells was upregulated after aTBI, which was reversed by propranolol administration in vivo and imitated by NE stimulation in vitro. Furthermore, the PD-1 blocker reversed the dysfunction of CD4⁺ and CD8⁺T cells in vitro. Conclusion: Our findings demonstrated that aTBI activated the SNS, and further upregulated the expression of PD-1 on CD4⁺ and CD8⁺ T cells, which, in turn, impaired their function and contributed to immunosuppression.

show abstract

Association of Childhood Family Connection With Flourishing in Young Adulthood Among Those With Type 1 Diabetes

et al. 2020

View full text Add to dashboard Cite

IMPORTANCE Higher levels of childhood family connection have been associated with measures of adult flourishing or eudaimonic well-being, such as purpose, self-acceptance, positive relationships, and growth. However, this association has not been examined among those with childhood-onset chronic disease. OBJECTIVES To investigate whether higher levels of childhood family connection were associated with greater flourishing in young adulthood among those with type 1 diabetes and, secondarily, whether this association was present across levels of adverse childhood experiences and childhood social position.

show abstract

Mechanisms and Therapeutic Relevance of Neuro-immune Communication

Cited by 480 publications

References 162 publications

Molecular and Functional Neuroscience in Immunity

Molecular and Functional Neuroscience in Immunity

Acute Traumatic Brain Injury Induces CD4<sup>+</sup> and CD8<sup>+</sup> T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

Association of Childhood Family Connection With Flourishing in Young Adulthood Among Those With Type 1 Diabetes

Contact Info

Product

Resources

About