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The neuro-immune balance in neuropathic pain: Involvement of inflammatory immune cells, immune-like glial cells and cytokines
Abstract
In a large proportion of individuals nervous system damage may lead to a debilitating chronic neuropathic pain. Such pain may now be considered a neuro-immune disorder, since recent data indicate a critical involvement of innate and adaptive immune responses following nerve injury. Activation of immune and immune-like glial cells in the injured nerve, dorsal root ganglia and spinal cord results in the release of both pro- and anti-inflammatory cytokines, as well as algesic and analgesic mediators, the balance of which determines whether pain chronicity is established. This review will critically examine the role of the immune system in modulating chronic pain in animal models of nervous system injury, and highlight the possible therapeutic opportunities to intervene in the development and maintenance of neuropathic pain.
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“Neuropathic pain pathophysiology is complex and includes functional alterations of the CNS and PNS (Cohen and Mao, 2014) in addition to neuro-immune interactions (Austin and Moalem-Taylor, 2010).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Austin and Moalem-Taylor, 2010
In the citing paper
“Five nights of partial sleep deprivation led to a reduction of stimulated IL-2 production in healthy humans (24), which is in line with the studies manipulating sleep for only one night.”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [24]
In the citing paper
“In addition, sleep, by favoring pro-inflammatory and Th1 cytokine production, further supports the interaction between APCs and T cells and the subsequent differentiation and proliferation of Th1 cells, eventually leading to the formation of IgG1 and IgG3 antibodies (24, 67, 148, 254, 320).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [24]
In the citing paper
“Such a shift in the Th1/Th2 balance has been also observed for alcohol dependence-associated sleep changes (462) and in response to experimental sleep deficiency (24, 320), and may explain lower vaccine efficacy and increased infection risk in the context of sleep deficiency”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [24]
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Metadata
- Authors
- Austin, P. J., & Moalem-Taylor, G.
- Affiliations
- UNSW Sydney (AU)
- Corresponding author
- Austin, Paul J.
- ORCID
- Austin, Paul J.
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2010-12
- Volume
- 229
- Issue
- 1-2
- Pages
- 26-50
- ISSN
- 0165-5728 (ISSN-L)
- OpenAlex
- W2111964682
- Semantic Scholar
- 1eb0fd50688ee519889d6649f4b3dbab6c461a2a
- Cited by
- 607
- References
- 401
- Citations by year
- 2026: 28 · 2025: 28 · 2024: 26 · 2023: 49 · 2022: 26 · 2021: 46 · 2020: 40 · 2019: 41 · 2018: 38 · 2017: 42 · 2016: 52 · 2015: 47 · 2014: 39 · 2013: 43 · 2012: 31
- FWCI
- 3.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroimmunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
- Keywords
- neuropathic pain, neuroimmune interactions, chronic pain, cytokines, dorsal root ganglia, spinal cord, nerve injury, pain chronicity
- MeSH terms
- Animals, Humans, Immune System, Inflammation, Nervous System, Neuralgia, Neuroglia, Cytokines
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