title: Cannabidiol inhibits pathogenic T cells, decreases spinal microglial activation and ameliorates multiple sclerosis-like disease in C57BL/6 mice.
abstract: OBJECTIVE
  Cannabis extracts and several cannabinoids have been shown to exert broad anti-inflammatory activities in experimental models of inflammatory CNS degenerative diseases. Clinical use of many cannabinoids is limited by their psychotropic effects. However, phytocannabinoids like cannabidiol (CBD), devoid of psychoactive activity, are, potentially, safe and effective alternatives for alleviating neuroinflammation and neurodegeneration.
  
  
  METHODS
  We used experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) in C57BL/6 mice, as a model of multiple sclerosis. Using immunocytochemistry and cell proliferation assays we evaluated the effects of CBD on microglial activation in MOG-immunized animals and on MOG-specific T-cell proliferation.
  
  
  RESULTS
  Treatment with CBD during disease onset ameliorated the severity of the clinical signs of EAE. This effect of CBD was accompanied by diminished axonal damage and inflammation as well as microglial activation and T-cell recruitment in the spinal cord of MOG-injected mice. Moreover, CBD inhibited MOG-induced T-cell proliferation in vitro at both low and high concentrations of the myelin antigen. This effect was not mediated via the known cannabinoid CB(1) and CB(2) receptors.
  
  
  CONCLUSIONS
  CBD, a non-psychoactive cannabinoid, ameliorates clinical signs of EAE in mice, immunized against MOG. Suppression of microglial activity and T-cell proliferation by CBD appeared to contribute to these beneficial effects.
authors: The Dr. Miriam and Sheldon G. Adelson Center for Biology of Addictive Diseases, Physiology and Pharmacology Department, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
authors: Ewa
authors: E
authors: Kozela
authors: Nirit
authors: N
authors: Lev
authors: Nathali
authors: N
authors: Kaushansky
authors: Raya
authors: R
authors: Eilam
authors: Neta
authors: N
authors: Rimmerman
authors: Rivka
authors: R
authors: Levy
authors: Avraham
authors: A
authors: Ben-Nun
authors: Ana
authors: A
authors: Juknat
authors: Zvi
authors: Z
authors: Vogel
mesh_terms: D000818:Animals; D002185:Cannabidiol / Q000494:pharmacology*; D020833:Diffuse Axonal Injury / Q000188:drug therapy; D004195:Disease Models, Animal; D018450:Disease Progression; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000139:chemically induced / Q000188:drug therapy; D005260:Female; D008264:Macrophages / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000187:drug effects*; D009103:Multiple Sclerosis / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D009185:Myelin Proteins / Q000494:pharmacology; D063308:Myelin-Oligodendrocyte Glycoprotein; D009410:Nerve Degeneration / Q000188:drug therapy; D013116:Spinal Cord / Q000187:drug effects*; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology
chemical_list: C571327:Mog protein, mouse; D009185:Myelin Proteins; D063308:Myelin-Oligodendrocyte Glycoprotein; D002185:Cannabidiol