Some sweet new research which was published Nov. 14, 2013, in the journal Cell Immunology discovered that by activating the human body’s cannabinoid receptors – thanks marijuana – the CB2 receptor alleviates EAE (Experimental autoimmune encephalomyelitis) by reducing Th17 differentiation and immune cell accumulation in the CNS.
Per the Journal’s report;” CB2, the cannabinoid receptor expressed primarily on hematopoietic cells and activated microglia, mediates the immunoregulatory functions of cannabinoids. The involvement of CB2 in EAE has been demonstrated by using both endogenous and exogenous ligands. We showed previously that CB2 selective agonists inhibit leukocyte rolling and adhesion to CNS microvasculature and ameliorate clinical symptom in both chronic and remitting-relapsing EAE models. Here we showed that Gp1a, a highly selective CB2 agonist, with a four log higher affinity for CB2 than CB1, reduced clinical scores and facilitated recovery in EAE in conjunction with long term reduction in demyelination and axonal loss.”
The study explains that; “This is the first report on the in vivo CB2-mediated Gp1a inhibition of Th17/Th1 differentiation.” Also noting that “the Gp1a-induced inhibition of Th17/Th1 differentiation in vitro, both in non-polarizing and polarizing conditions — as well as The CB2-induced inhibition of Th17 differentiation are highly relevant in view of recent studies emphasizing the importance of pathogenic self-reactive Th17 cells in EAE/MS. In addition, the combined effect on Th17 differentiation and immune cell accumulation into the CNS, emphasize the relevance of CB2 selective ligands as potential therapeutic agents in neuroinflammation.”