A new study published in the journal Cell Immunology has found that activation of the body’s cannabinoid receptors – something done naturally by cannabis and cannabinoids – has neuroinflammatory capabilities.
According to the study; “Here we showed that Gp1a, a highly selective CB2 [cannabinoid receptor 2] agonist, with a four log higher affinity for CB2 than CB1, reduced clinical scores and facilitated recovery in EAE [experimental autoimmune encephalomyelitis, a disease of the central nervous system] in conjunction with long term reduction in demyelination and axonal loss.”
The study continues; “This is the first report on the in vivo CB2-mediated Gp1a inhibition of Th17/Th1 differentiation. We also confirmed the Gp1a-induced inhibition of Th17/Th1 differentiation in vitro, both in non-polarizing and polarizing conditions. The CB2-induced inhibition of Th17 differentiation is highly relevant in view of recent studies emphasizing the importance of pathogenic self-reactive Th17 cells in EAE/MS.
Researchers conclude that “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.”
The study was conducted by researchers at the Temple University School of Medicine in Philadelphia.