Cannabidiol Attenuates Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis Through Induction of Myeloid-Derived Suppressor Cells
Year: 2018
Type: article
Abstract: Multiple Sclerosis (MS) is a chronic debilitating autoimmune disease without a cure. While the use of marijuana cannabinoids for MS has recently been approved in some countries, the precise mechanism of action leading to attenuate neuroinflammation, is not clear. We used experimental autoimmune encephalomyelitis (EAE), a murine model of MS, to explore the anti-inflammatory properties of cannabidiol (CBD), a non-psychoactive cannabinoid. Treatment with CBD caused attenuation of EAE disease paradigms as indicated by a significant reduction in clinical scores of paralysis, decreased T cell infiltration in the CNS, and reduced levels of IL-17 and IFN. Interestingly, CBD treatment led to a profound increase in Myeloid Derived Suppressor Cells (MDSC) in EAE mice when compared to the vehicle-treated EAE controls. These MDSCs caused robust inhibition of MOG-induced proliferation of T cells in vitro. Moreover, adoptive transfer of CBD-induced MDSCs ameliorated EAE while MDSC depletion reversed the beneficial effects of CBD treatment, thereby conclusively demonstrating that MDSCs played a crucial role in CBD-mediated attenuation of EAE. Together, these studies demonstrate for the first time that CBD treatment may ameliorate EAE through induction of immunosuppressive MDSCs.
Source: Frontiers in Immunology
Authors: David M. Elliott, Narendra Singh, Mitzi Nagarkatti, Prakash S. Nagarkatti
Institution: University of South Carolina
Language: English
Subfield: Pathology and Forensic Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,801
Awards: Immunopathological basis of PTSD, Role of natural indoles in experimental autoimmune encephalomyelitis, G4323986160, G58725747, Epigenetic Mechanisms of T Cell Dysregulation in PTSD, AhR ligands in epigenetic dysregulation of T cells, Estrogen-T cell Interactions, G9000020609, G9000126961, G9000293411
OpenAlex ID: W2887820457
