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Emerging role of the cannabinoid receptor CB 2 in immune regulation: therapeutic prospects for neuroinflammation
Open accessAbstract
There is now a large body of data indicating that the cannabinoid receptor type 2 (CB 2 ) is linked to a variety of immune events. This functional relevance appears to be most salient in the course of inflammation, a process during which there is an increased number of receptors that are available for activation. Studies aimed at elucidating signal transduction events resulting from CB 2 interaction with its native ligands, and of the role of exogenous cannabinoids in modulating this process, are providing novel insights into the role of CB 2 in maintaining a homeostatic immune balance within the host. Furthermore, these studies suggest that the CB 2 may serve as a selective molecular target for therapeutic manipulation of untoward immune responses, including those associated with a variety of neuropathies that exhibit a hyperinflammatory component.
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“Endocannabinoids mediate inflammation by regulating cytokines at different steps throughout the inflammatory response (Cabral and Griffin-Thomas, 2009).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Cabral and Griffin-Thomas, 2009
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“For example, THC and AEA suppress proinflammatory cytokines and enhance anti-inflammatory cytokines in both innate and adaptive immune responses (Cabral and Griffin-Thomas, 2009).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Cabral and Griffin-Thomas, 2009
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“Cannabinoids also inhibit the cell-specific proliferation of B and T cells (Cabral and Griffin-Thomas, 2009;Klein and Cabral, 2006).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Cabral and Griffin-Thomas, 2009
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Research works printed but not linked: 4
- http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=105400 (amyotrophic lateral sclerosis)
- http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=114610 (CB1)
- http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=605051 (CB2) The National Institute of Drug Abuse website includes listings of clinical trials:
- http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=126200 (multiple sclerosis)
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Metadata
- Authors
- Cabral, G. A., & Griffin-Thomas, L.
- Affiliations
- Virginia Commonwealth University (US)
- Corresponding author
- Cabral, Guy A.
- Venue
- Expert Reviews in Molecular Medicine
- Publisher
- Cambridge University Press (CUP)
- Published
- 2009-01
- Volume
- 11
- Pages
- e3-e3
- ISSN
- 1462-3994 (ISSN-L)
- PMC
- PMC2768535
- OpenAlex
- W2023366312
- Cited by
- 408
- References
- 190
- Citations by year
- 2026: 25 · 2025: 37 · 2024: 22 · 2023: 24 · 2022: 23 · 2021: 29 · 2020: 34 · 2019: 24 · 2018: 28 · 2017: 37 · 2016: 13 · 2015: 15 · 2014: 22 · 2013: 22 · 2012: 17
- FWCI
- 1.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Expert Reviews in Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of Cambridge
- National Institutes of Health
- National Institute on Drug Abuse (DA005832, R01DA005832, R01DA029532)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Cannabis and Cannabinoid Research
- Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
- Keywords
- CB2 receptor, immune regulation, neuroinflammation, signal transduction, exogenous cannabinoids, immune homeostasis, neuropathy, hyperinflammation, therapeutic target
- MeSH terms
- Amino Acid Sequence, Animals, Humans, Inflammation, Molecular Sequence Data, Nervous System, Research, Neuroimmunomodulation, Receptor, Cannabinoid, CB2
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